rabbit anti cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cxcr5
    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and <t>CXCR5</t> (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.
    Rabbit Anti Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury"

    Article Title: Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury

    Journal: Frontiers in Genetics

    doi: 10.3389/fgene.2022.946524

    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.
    Figure Legend Snippet: mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.

    Techniques Used: Expressing

    rabbit anti cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cxcr5
    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and <t>CXCR5</t> (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.
    Rabbit Anti Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti cxcr5/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti cxcr5 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury"

    Article Title: Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury

    Journal: Frontiers in Genetics

    doi: 10.3389/fgene.2022.946524

    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.
    Figure Legend Snippet: mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.

    Techniques Used: Expressing

    72172s  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 72172s

    72172s, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/72172s/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    72172s - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma"

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    Journal: iScience

    doi: 10.1016/j.isci.2022.103883


    Figure Legend Snippet:

    Techniques Used: Recombinant, Software

    rabbit anti cxcr5 monoclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cxcr5 monoclonal antibody
    TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers <t>(CXCR5</t> and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas
    Rabbit Anti Cxcr5 Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti cxcr5 monoclonal antibody/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    rabbit anti cxcr5 monoclonal antibody - by Bioz Stars, 2023-02
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    Images

    1) Product Images from "Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma"

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    Journal: iScience

    doi: 10.1016/j.isci.2022.103883

    TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers (CXCR5 and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas
    Figure Legend Snippet: TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers (CXCR5 and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas

    Techniques Used: Expressing, Staining

    Treg recruitment as potential mechanism of decreased CD8 + T cell infiltration in tertiary lymphoid structures (A) Comparison of immune suppressive cell infiltration estimated from XCELL between MIA tumor and adjacent normal tissues. p values are calculated using Mann-Whitney U test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (B) Plot of Tfr/Tfh marker ratio vs CD8 + T cell infiltration. FoxP3, PDCD1, and IL2RA are markers of Tfr cells, while BCL6, ICOS, and IL7R are markers of Tfh cells. See text. p values are calculated using Spearman correlation test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA 7-plex panel staining for Tfr and Tfh. Merged multispectral image was captured after 6-cycle TSA staining and DAPI counterstain and reveals a mature TLS architecture. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, FOXP3: red, BCL6: cyan and CD3: orange. Sub-populations of CD4 + T cells are highlighted by arrows (Tfr: red, Treg: purple, Th: green and Tfh: cyan). (D) Paired comparison of CD8 + T cell density between non-follicle (Non-Fol) and TLS areas. (E) Paired comparison of ratio of regulatory T cells to helper T cells between TLS and non-follicle areas. (F) Comparison of CD8 + T cell density between groups with high and low Tfr/Tfh ratio
    Figure Legend Snippet: Treg recruitment as potential mechanism of decreased CD8 + T cell infiltration in tertiary lymphoid structures (A) Comparison of immune suppressive cell infiltration estimated from XCELL between MIA tumor and adjacent normal tissues. p values are calculated using Mann-Whitney U test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (B) Plot of Tfr/Tfh marker ratio vs CD8 + T cell infiltration. FoxP3, PDCD1, and IL2RA are markers of Tfr cells, while BCL6, ICOS, and IL7R are markers of Tfh cells. See text. p values are calculated using Spearman correlation test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA 7-plex panel staining for Tfr and Tfh. Merged multispectral image was captured after 6-cycle TSA staining and DAPI counterstain and reveals a mature TLS architecture. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, FOXP3: red, BCL6: cyan and CD3: orange. Sub-populations of CD4 + T cells are highlighted by arrows (Tfr: red, Treg: purple, Th: green and Tfh: cyan). (D) Paired comparison of CD8 + T cell density between non-follicle (Non-Fol) and TLS areas. (E) Paired comparison of ratio of regulatory T cells to helper T cells between TLS and non-follicle areas. (F) Comparison of CD8 + T cell density between groups with high and low Tfr/Tfh ratio

    Techniques Used: MANN-WHITNEY, Marker, Staining


    Figure Legend Snippet:

    Techniques Used: Recombinant, Software

    rabbit anti cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cxcr5
    qPCR and Immunohistochemical to detect the expression of <t>CXCR5</t> in ccRCC tissues. A TCGA database and our hospital database detect the relationship between CXCR5mRNA expression and ccRCC clinicopathological characteristics. B TCGA database and our hospital database to detect the relationship between CXCR5mRNA expression and ccRCC prognosis. C Immunohistochemical staining of CXCR5 protein in ccRCC tissues and adjacent tissues
    Rabbit Anti Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti cxcr5/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti cxcr5 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "M2 macrophages secrete CXCL13 to promote renal cell carcinoma migration, invasion, and EMT"

    Article Title: M2 macrophages secrete CXCL13 to promote renal cell carcinoma migration, invasion, and EMT

    Journal: Cancer Cell International

    doi: 10.1186/s12935-021-02381-1

    qPCR and Immunohistochemical to detect the expression of CXCR5 in ccRCC tissues. A TCGA database and our hospital database detect the relationship between CXCR5mRNA expression and ccRCC clinicopathological characteristics. B TCGA database and our hospital database to detect the relationship between CXCR5mRNA expression and ccRCC prognosis. C Immunohistochemical staining of CXCR5 protein in ccRCC tissues and adjacent tissues
    Figure Legend Snippet: qPCR and Immunohistochemical to detect the expression of CXCR5 in ccRCC tissues. A TCGA database and our hospital database detect the relationship between CXCR5mRNA expression and ccRCC clinicopathological characteristics. B TCGA database and our hospital database to detect the relationship between CXCR5mRNA expression and ccRCC prognosis. C Immunohistochemical staining of CXCR5 protein in ccRCC tissues and adjacent tissues

    Techniques Used: Immunohistochemical staining, Expressing, Staining

    Correlation between  CXCR5  expression and clinical characteristics of ccRCC patients
    Figure Legend Snippet: Correlation between CXCR5 expression and clinical characteristics of ccRCC patients

    Techniques Used: Expressing

    cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cxcr5
    Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or <t>CXCR5</t> −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type
    Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cxcr5/product/Cell Signaling Technology Inc
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    Images

    1) Product Images from "CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway"

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-021-02300-1

    Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or CXCR5 −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type
    Figure Legend Snippet: Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or CXCR5 −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type

    Techniques Used: Ligation, Small Interfering RNA

    Cognitive deficits and up-regulation of CXCR5 in a mouse model of sepsis-associated encephalopathy. Adult male C57BL/6 J mice were subjected to sham surgery or CLP. a Escape latency time, b time spent in the target quadrant, and c number of crossings over the target quadrant in the Morris water maze beginning on day 14 after CLP. d Freezing time in the fear conditioning test on day 19 after CLP ( n = 16 per group). e, f Western blot and densitometry of hippocampal CXCR5 on days 3, 7 and 14 after CLP ( n = 4 per group). GAPDH was used as an internal control. g Double staining of CXCR5 with microglia marker Iba-1 in the hippocampus at 14 days after CLP. Arrows indicate double-stained cells. Magnification, 200 × . Scale bar, 100 μm. h Quantification of immunofluorescent cells co-staining positive for CXCR5 and Iba-1. * p < 0.05 vs. sham. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1
    Figure Legend Snippet: Cognitive deficits and up-regulation of CXCR5 in a mouse model of sepsis-associated encephalopathy. Adult male C57BL/6 J mice were subjected to sham surgery or CLP. a Escape latency time, b time spent in the target quadrant, and c number of crossings over the target quadrant in the Morris water maze beginning on day 14 after CLP. d Freezing time in the fear conditioning test on day 19 after CLP ( n = 16 per group). e, f Western blot and densitometry of hippocampal CXCR5 on days 3, 7 and 14 after CLP ( n = 4 per group). GAPDH was used as an internal control. g Double staining of CXCR5 with microglia marker Iba-1 in the hippocampus at 14 days after CLP. Arrows indicate double-stained cells. Magnification, 200 × . Scale bar, 100 μm. h Quantification of immunofluorescent cells co-staining positive for CXCR5 and Iba-1. * p < 0.05 vs. sham. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1

    Techniques Used: Western Blot, Double Staining, Marker, Staining, Ligation, Binding Assay

    CXCR5 knockout ameliorated sepsis-induced cognitive dysfunction in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and b densitometry of hippocampal CXCR5 on day 14 after CLP. GAPDH was used as an internal control ( n = 4 per group). Mice were assessed in the Morris water maze on day 14 after CLP, followed by the fear conditioning test. c Escape latency time, d time spent in the target quadrant, and e number of crossings over the target quadrant in the Morris water maze. f Freezing time in the fear conditioning test ( n = 16 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, WT wild-type
    Figure Legend Snippet: CXCR5 knockout ameliorated sepsis-induced cognitive dysfunction in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and b densitometry of hippocampal CXCR5 on day 14 after CLP. GAPDH was used as an internal control ( n = 4 per group). Mice were assessed in the Morris water maze on day 14 after CLP, followed by the fear conditioning test. c Escape latency time, d time spent in the target quadrant, and e number of crossings over the target quadrant in the Morris water maze. f Freezing time in the fear conditioning test ( n = 16 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, WT wild-type

    Techniques Used: Knock-Out, Western Blot, Ligation

    CXCR5 knockout restored hippocampal autophagy in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Representative transmission electron micrographs of the hippocampus show zoomed-in views (magnification, 5000 × ; Scale bar, 500 nm) of full image of a cell (magnification, 2000 × ; Scale bar, 2000 nm). Arrows indicate autophagosome. b Representative immunofluorescence micrographs showing LC3 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. c Quantification of immunofluorescent cells staining positive for LC3. d – h Western blot and densitometry of hippocampal LC3, beclin-1, Atg-5 and p62, and the ratio of LC3-II/LC3-I. GAPDH was used as an internal control ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Atg-5 autophagy-related gene-5, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3, WT wild-type
    Figure Legend Snippet: CXCR5 knockout restored hippocampal autophagy in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Representative transmission electron micrographs of the hippocampus show zoomed-in views (magnification, 5000 × ; Scale bar, 500 nm) of full image of a cell (magnification, 2000 × ; Scale bar, 2000 nm). Arrows indicate autophagosome. b Representative immunofluorescence micrographs showing LC3 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. c Quantification of immunofluorescent cells staining positive for LC3. d – h Western blot and densitometry of hippocampal LC3, beclin-1, Atg-5 and p62, and the ratio of LC3-II/LC3-I. GAPDH was used as an internal control ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Atg-5 autophagy-related gene-5, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3, WT wild-type

    Techniques Used: Knock-Out, Transmission Assay, Immunofluorescence, Staining, Western Blot, Ligation

    CXCR5 knockout reversed the alteration in hippocampal microglial M1/M2 polarization in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and densitometry of hippocampal Iba-1 on day 14 after CLP. b Representative micrographs of immunohistochemistry for Iba-1 in the hippocampal CA1 and the number of Iba-1-positive cells. Magnification, 200 × . Scale bar, 100 μm. Representative immunofluorescence micrographs and quantitation ( n = 4 per group) after staining for c M1 marker iNOS and d M2 marker Arg-1 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Arg-1 arginase-1, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, Iba-1 ionized calcium binding adaptor molecule-1, iNOS inducible nitric oxide synthase, WT wild-type
    Figure Legend Snippet: CXCR5 knockout reversed the alteration in hippocampal microglial M1/M2 polarization in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and densitometry of hippocampal Iba-1 on day 14 after CLP. b Representative micrographs of immunohistochemistry for Iba-1 in the hippocampal CA1 and the number of Iba-1-positive cells. Magnification, 200 × . Scale bar, 100 μm. Representative immunofluorescence micrographs and quantitation ( n = 4 per group) after staining for c M1 marker iNOS and d M2 marker Arg-1 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Arg-1 arginase-1, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, Iba-1 ionized calcium binding adaptor molecule-1, iNOS inducible nitric oxide synthase, WT wild-type

    Techniques Used: Knock-Out, Western Blot, Immunohistochemistry, Immunofluorescence, Quantitation Assay, Staining, Marker, Ligation, Binding Assay

    CXCR5 knockout decreased hippocampal p-p38MAPK, IL-1β and IL-6 levels in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a – d Western blot and densitometry of hippocampal p-p38MAPK, p38MAPK, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, p38MAPK mitogen-activated protein kinase, p-p38MAPK phosphorylated p38MAPK, WT wild-type
    Figure Legend Snippet: CXCR5 knockout decreased hippocampal p-p38MAPK, IL-1β and IL-6 levels in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a – d Western blot and densitometry of hippocampal p-p38MAPK, p38MAPK, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, p38MAPK mitogen-activated protein kinase, p-p38MAPK phosphorylated p38MAPK, WT wild-type

    Techniques Used: Knock-Out, Western Blot, Ligation

    CXCR5 knockdown restored p38MAPK-dependent autophagy in LPS-treated microglial cultures. Microglial cells were treated with CXCR5 siRNA. a Western blot and densitometry of CXCR5 in microglia at 24 h after CXCR5 siRNA administration. $ p < 0.05 vs. cells treated without siRNAs. Microglial cells were treated with CXCR5 siRNA at 24 h before LPS treatment. Some cultures were also treated with p38MAPK inhibitor SB203580 or agonist P79350 at 1 h before siRNA administration. b Representative micrographs of immunohistochemistry for LC3 in microglia at 24 h after LPS treatment. Magnification, 200 × . Scale bar, 100 μm. c Calculation of LC3-positive area. d – h Western blot and densitometry of LC3, beclin-1, Atg-5 and p62, and the ratio LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. Atg-5 autophagy-related gene-5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3
    Figure Legend Snippet: CXCR5 knockdown restored p38MAPK-dependent autophagy in LPS-treated microglial cultures. Microglial cells were treated with CXCR5 siRNA. a Western blot and densitometry of CXCR5 in microglia at 24 h after CXCR5 siRNA administration. $ p < 0.05 vs. cells treated without siRNAs. Microglial cells were treated with CXCR5 siRNA at 24 h before LPS treatment. Some cultures were also treated with p38MAPK inhibitor SB203580 or agonist P79350 at 1 h before siRNA administration. b Representative micrographs of immunohistochemistry for LC3 in microglia at 24 h after LPS treatment. Magnification, 200 × . Scale bar, 100 μm. c Calculation of LC3-positive area. d – h Western blot and densitometry of LC3, beclin-1, Atg-5 and p62, and the ratio LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. Atg-5 autophagy-related gene-5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3

    Techniques Used: Western Blot, Immunohistochemistry

    CXCR5 knockdown reversed the alteration of p38MAPK-dependent microglial M1/M2 polarization and production of inflammatory cytokines in LPS-treated microglial cultures. a Representative micrographs of immunohistochemistry for Iba-1 in the microglia. Magnification, 200 × . Scale bar, 100 μm. b Calculation of Iba-1-positive area. c – h Western blot and densitometry of Iba-1, CD86, CD206, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin-1β, IL-6 interleukin-6, LPS lipopolysaccharide
    Figure Legend Snippet: CXCR5 knockdown reversed the alteration of p38MAPK-dependent microglial M1/M2 polarization and production of inflammatory cytokines in LPS-treated microglial cultures. a Representative micrographs of immunohistochemistry for Iba-1 in the microglia. Magnification, 200 × . Scale bar, 100 μm. b Calculation of Iba-1-positive area. c – h Western blot and densitometry of Iba-1, CD86, CD206, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin-1β, IL-6 interleukin-6, LPS lipopolysaccharide

    Techniques Used: Immunohistochemistry, Western Blot, Binding Assay

    CXCR5 knockdown inhibited activation of p38MAPK-dependent NF-κB/STAT3 signaling in LPS-treated microglial cultures. a – d Western blot and densitometry of p-p38MAPK, p38MAPK, p-NF-κB, NF-κB, p-STAT3 and STAT3 and relevant ratios ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK p38 mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription
    Figure Legend Snippet: CXCR5 knockdown inhibited activation of p38MAPK-dependent NF-κB/STAT3 signaling in LPS-treated microglial cultures. a – d Western blot and densitometry of p-p38MAPK, p38MAPK, p-NF-κB, NF-κB, p-STAT3 and STAT3 and relevant ratios ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK p38 mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Techniques Used: Activation Assay, Western Blot

    Autophagy inhibition attenuated the effects of CXCR5 knockdown on microglial polarization and inflammatory cytokines production in LPS-treated microglial cultures. a – g Western blot and densitometry of LC3, Iba-1, CD86, and CD206, IL-1β, IL-6 and the ratio of LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, 3-MA 3-methyladenine
    Figure Legend Snippet: Autophagy inhibition attenuated the effects of CXCR5 knockdown on microglial polarization and inflammatory cytokines production in LPS-treated microglial cultures. a – g Western blot and densitometry of LC3, Iba-1, CD86, and CD206, IL-1β, IL-6 and the ratio of LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, 3-MA 3-methyladenine

    Techniques Used: Inhibition, Western Blot, Binding Assay

    Schematic diagram depicting the possible mechanisms through which CXCR5 regulates autophagy. MAPK signaling downstream of CXCR5 induced by LPS promotes the up-regulation of NF-κB/STAT3 axis. Consequently, activation of NF-κB/STAT3 pathway contributes to incomplete activation of autophagy and production of inflammatory cytokines, thereby impairs learning and memory function. CXCR5 down-regulation results in inhibition of MAPK/NF-κB/STAT3 axis and activation of autophagy in brain, which leads to the improved cognitive function in mice with sepsis-associated encephalopathy. Atg-5 autophagy-related gene-5, CXCR5 C-X-C chemokine receptor type 5, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription
    Figure Legend Snippet: Schematic diagram depicting the possible mechanisms through which CXCR5 regulates autophagy. MAPK signaling downstream of CXCR5 induced by LPS promotes the up-regulation of NF-κB/STAT3 axis. Consequently, activation of NF-κB/STAT3 pathway contributes to incomplete activation of autophagy and production of inflammatory cytokines, thereby impairs learning and memory function. CXCR5 down-regulation results in inhibition of MAPK/NF-κB/STAT3 axis and activation of autophagy in brain, which leads to the improved cognitive function in mice with sepsis-associated encephalopathy. Atg-5 autophagy-related gene-5, CXCR5 C-X-C chemokine receptor type 5, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Techniques Used: Activation Assay, Inhibition

    cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cxcr5
    a The dot plot summarizing the cell–cell interactions among CD8-C2 (T RM -like), B, and CD4-C9 (T FH -like) cells by CellPhoneDB analysis. Only significant ligand–receptor interactions are presented here. The size of the circle indicates the statistical significance, and the color gradient indicates the mean expression value of gene pairs. b Representative multiplexed immunofluorescence (IF) of TLS-like lesion in EGFR-WT ( n = 14) (upper) (scale bar 100 μm: left, scale bars 50 μm: right magnified) and EGFR-MT ( n = 14) (lower) (scale bar 100 μm: left, scale bars 50 μm: right magnified) tumors. Summarized graph for the area of TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) tumors for single-cell analysis (** p ≤ 0.005, two-sided test) (upper panel) and in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation (* p ≤ 0.05, two-sided test) (lower panel). c Representative multiplexed IF of CD4, CXCL13, CD103, CD8, <t>CXCR5,</t> and CD20 in tumor specimens from EGFR-WT ( n = 14) (left) (scale bar 100 μm) and EGFR-MT ( n = 14) (right) (scale bar 100 μm) patients. d Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) patients. The number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells are significantly higher in EGFR-WT than EGFR-MT (* p ≤ 0.05, ** p ≤ 0.005, two-sided test). e Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation. Consistently, the number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells were significantly higher in EGFR-WT than EGFR-MT (** p ≤ 0.005, *** p ≤ 0.0005, two-sided test). f An illustrative summary of the proposed model for T FH –B–T RM lymphocyte cooperation in TLS for antitumor immunity in lung cancer. Data are represented as mean ± SEM. Source data are provided as a Source Data file.
    Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Dysregulation of T FH -B-T RM lymphocyte cooperation is associated with unfavorable anti-PD-1 responses in EGFR -mutant lung cancer"

    Article Title: Dysregulation of T FH -B-T RM lymphocyte cooperation is associated with unfavorable anti-PD-1 responses in EGFR -mutant lung cancer

    Journal: Nature Communications

    doi: 10.1038/s41467-021-26362-0

    a The dot plot summarizing the cell–cell interactions among CD8-C2 (T RM -like), B, and CD4-C9 (T FH -like) cells by CellPhoneDB analysis. Only significant ligand–receptor interactions are presented here. The size of the circle indicates the statistical significance, and the color gradient indicates the mean expression value of gene pairs. b Representative multiplexed immunofluorescence (IF) of TLS-like lesion in EGFR-WT ( n = 14) (upper) (scale bar 100 μm: left, scale bars 50 μm: right magnified) and EGFR-MT ( n = 14) (lower) (scale bar 100 μm: left, scale bars 50 μm: right magnified) tumors. Summarized graph for the area of TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) tumors for single-cell analysis (** p ≤ 0.005, two-sided test) (upper panel) and in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation (* p ≤ 0.05, two-sided test) (lower panel). c Representative multiplexed IF of CD4, CXCL13, CD103, CD8, CXCR5, and CD20 in tumor specimens from EGFR-WT ( n = 14) (left) (scale bar 100 μm) and EGFR-MT ( n = 14) (right) (scale bar 100 μm) patients. d Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) patients. The number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells are significantly higher in EGFR-WT than EGFR-MT (* p ≤ 0.05, ** p ≤ 0.005, two-sided test). e Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation. Consistently, the number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells were significantly higher in EGFR-WT than EGFR-MT (** p ≤ 0.005, *** p ≤ 0.0005, two-sided test). f An illustrative summary of the proposed model for T FH –B–T RM lymphocyte cooperation in TLS for antitumor immunity in lung cancer. Data are represented as mean ± SEM. Source data are provided as a Source Data file.
    Figure Legend Snippet: a The dot plot summarizing the cell–cell interactions among CD8-C2 (T RM -like), B, and CD4-C9 (T FH -like) cells by CellPhoneDB analysis. Only significant ligand–receptor interactions are presented here. The size of the circle indicates the statistical significance, and the color gradient indicates the mean expression value of gene pairs. b Representative multiplexed immunofluorescence (IF) of TLS-like lesion in EGFR-WT ( n = 14) (upper) (scale bar 100 μm: left, scale bars 50 μm: right magnified) and EGFR-MT ( n = 14) (lower) (scale bar 100 μm: left, scale bars 50 μm: right magnified) tumors. Summarized graph for the area of TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) tumors for single-cell analysis (** p ≤ 0.005, two-sided test) (upper panel) and in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation (* p ≤ 0.05, two-sided test) (lower panel). c Representative multiplexed IF of CD4, CXCL13, CD103, CD8, CXCR5, and CD20 in tumor specimens from EGFR-WT ( n = 14) (left) (scale bar 100 μm) and EGFR-MT ( n = 14) (right) (scale bar 100 μm) patients. d Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 5) and EGFR-MT ( n = 4) patients. The number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells are significantly higher in EGFR-WT than EGFR-MT (* p ≤ 0.05, ** p ≤ 0.005, two-sided test). e Summarized graph for the numbers of each cell type in total TLS-like lesions in EGFR-WT ( n = 9) and EGFR-MT ( n = 10) tumors from independent patients for validation. Consistently, the number of CD4 + , CXCL13 + CD4 + T cells, CD8 + T cells, CD103 + CD8 + T cells were significantly higher in EGFR-WT than EGFR-MT (** p ≤ 0.005, *** p ≤ 0.0005, two-sided test). f An illustrative summary of the proposed model for T FH –B–T RM lymphocyte cooperation in TLS for antitumor immunity in lung cancer. Data are represented as mean ± SEM. Source data are provided as a Source Data file.

    Techniques Used: Expressing, Immunofluorescence, Single-cell Analysis

    cxcr5  (Cell Signaling Technology Inc)


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    a viSNE plots of B cells collected from non-inflamed and inflamed tonsils, HPV+ and HPV− HNSCC TIL and paired PBL (Supplementary Fig. ) were analyzed using Cytobank. Non-inflamed tonsil ( n = 4), inflamed tonsil ( n = 6), HPV + HNSCC ( n = 3), HPV− HNSCC ( n = 2). Bar plot displaying frequencies of GC B cells and plasma cells in non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 9), HPV− HNSCC ( n = 9). * P = 0.02 Student‘s 2-sided t test. b Bar plot for frequency of B cell subpopulations. Non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 12), HPV− HNSCC ( n = 13). ** P = 0.004, *** P = 0.0009, * P = 0.03, One way ANOVA followed by Tukey’s multiple comparisons test. c Frequencies of T follicular helper (T FH ), regulatory T follicular helper (T FHreg ), regulatory T cell (T reg ), T helper type 1 (T H 1) and CD8 T cells in non-inflamed tonsil ( n = 6), inflamed tonsils ( n = 10), HPV+ TIL ( n = 7), HPV− TIL ( n = 8). * P = 0.01,** P = 0.009,**** P < 0.0001. * P = 0.04, * P = 0.03, **** P < 0.0001. One-way ANOVA followed by Tukey’s multiple comparisons test. d Representative CD20+ IHC on HPV+ and HPV− HNSCC tumors (×4 magnification). e B cell infiltrate counted within tumor bed compared to TLS. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. **** P < 0.0001, Student‘s 2-sided t test. f Tumor TLS by site within the oropharynx (tonsil vs. tongue). Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. ** P = 0.0096, Student‘s 2-sided. Data are presented as mean values ± SEM. g Total number of tumor TLS and non-tumor TLS numbers in HPV+ and HPV− disease. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. * P = 0.0249, Student‘s 2-sided t test. Data are presented as mean values ± SEM. h Correlation of CD20 + tumor TLS with tumor area. Total tumor area (mm ) for each patient tumor was calculated by a pathologist. * P < 0.05, non-parametric Spearman correlation. i Total tumor TLS independently counted for CD20 + and CD4 + ( n = 50, 25 HPV+, 25 HPV−). **** P < 0.0001, *** P < 0.001, non-parametric Spearman correlation. j Total <t>CXCR5</t> was scored for all cell types ( n = 50, 25 HPV+, 25 HPV−).** P = 0.0012, Student‘s 2 sided t test. Source data are provided as a Source Data file.
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    1) Product Images from "B cell signatures and tertiary lymphoid structures contribute to outcome in head and neck squamous cell carcinoma"

    Article Title: B cell signatures and tertiary lymphoid structures contribute to outcome in head and neck squamous cell carcinoma

    Journal: Nature Communications

    doi: 10.1038/s41467-021-23355-x

    a viSNE plots of B cells collected from non-inflamed and inflamed tonsils, HPV+ and HPV− HNSCC TIL and paired PBL (Supplementary Fig. ) were analyzed using Cytobank. Non-inflamed tonsil ( n = 4), inflamed tonsil ( n = 6), HPV + HNSCC ( n = 3), HPV− HNSCC ( n = 2). Bar plot displaying frequencies of GC B cells and plasma cells in non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 9), HPV− HNSCC ( n = 9). * P = 0.02 Student‘s 2-sided t test. b Bar plot for frequency of B cell subpopulations. Non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 12), HPV− HNSCC ( n = 13). ** P = 0.004, *** P = 0.0009, * P = 0.03, One way ANOVA followed by Tukey’s multiple comparisons test. c Frequencies of T follicular helper (T FH ), regulatory T follicular helper (T FHreg ), regulatory T cell (T reg ), T helper type 1 (T H 1) and CD8 T cells in non-inflamed tonsil ( n = 6), inflamed tonsils ( n = 10), HPV+ TIL ( n = 7), HPV− TIL ( n = 8). * P = 0.01,** P = 0.009,**** P < 0.0001. * P = 0.04, * P = 0.03, **** P < 0.0001. One-way ANOVA followed by Tukey’s multiple comparisons test. d Representative CD20+ IHC on HPV+ and HPV− HNSCC tumors (×4 magnification). e B cell infiltrate counted within tumor bed compared to TLS. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. **** P < 0.0001, Student‘s 2-sided t test. f Tumor TLS by site within the oropharynx (tonsil vs. tongue). Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. ** P = 0.0096, Student‘s 2-sided. Data are presented as mean values ± SEM. g Total number of tumor TLS and non-tumor TLS numbers in HPV+ and HPV− disease. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. * P = 0.0249, Student‘s 2-sided t test. Data are presented as mean values ± SEM. h Correlation of CD20 + tumor TLS with tumor area. Total tumor area (mm ) for each patient tumor was calculated by a pathologist. * P < 0.05, non-parametric Spearman correlation. i Total tumor TLS independently counted for CD20 + and CD4 + ( n = 50, 25 HPV+, 25 HPV−). **** P < 0.0001, *** P < 0.001, non-parametric Spearman correlation. j Total CXCR5 was scored for all cell types ( n = 50, 25 HPV+, 25 HPV−).** P = 0.0012, Student‘s 2 sided t test. Source data are provided as a Source Data file.
    Figure Legend Snippet: a viSNE plots of B cells collected from non-inflamed and inflamed tonsils, HPV+ and HPV− HNSCC TIL and paired PBL (Supplementary Fig. ) were analyzed using Cytobank. Non-inflamed tonsil ( n = 4), inflamed tonsil ( n = 6), HPV + HNSCC ( n = 3), HPV− HNSCC ( n = 2). Bar plot displaying frequencies of GC B cells and plasma cells in non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 9), HPV− HNSCC ( n = 9). * P = 0.02 Student‘s 2-sided t test. b Bar plot for frequency of B cell subpopulations. Non-inflamed tonsil ( n = 9), inflamed tonsil ( n = 16), HPV+ HNSCC ( n = 12), HPV− HNSCC ( n = 13). ** P = 0.004, *** P = 0.0009, * P = 0.03, One way ANOVA followed by Tukey’s multiple comparisons test. c Frequencies of T follicular helper (T FH ), regulatory T follicular helper (T FHreg ), regulatory T cell (T reg ), T helper type 1 (T H 1) and CD8 T cells in non-inflamed tonsil ( n = 6), inflamed tonsils ( n = 10), HPV+ TIL ( n = 7), HPV− TIL ( n = 8). * P = 0.01,** P = 0.009,**** P < 0.0001. * P = 0.04, * P = 0.03, **** P < 0.0001. One-way ANOVA followed by Tukey’s multiple comparisons test. d Representative CD20+ IHC on HPV+ and HPV− HNSCC tumors (×4 magnification). e B cell infiltrate counted within tumor bed compared to TLS. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. **** P < 0.0001, Student‘s 2-sided t test. f Tumor TLS by site within the oropharynx (tonsil vs. tongue). Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. ** P = 0.0096, Student‘s 2-sided. Data are presented as mean values ± SEM. g Total number of tumor TLS and non-tumor TLS numbers in HPV+ and HPV− disease. Total numbers from n = 50, 25 HPV+, 25 HPV− were graphed. * P = 0.0249, Student‘s 2-sided t test. Data are presented as mean values ± SEM. h Correlation of CD20 + tumor TLS with tumor area. Total tumor area (mm ) for each patient tumor was calculated by a pathologist. * P < 0.05, non-parametric Spearman correlation. i Total tumor TLS independently counted for CD20 + and CD4 + ( n = 50, 25 HPV+, 25 HPV−). **** P < 0.0001, *** P < 0.001, non-parametric Spearman correlation. j Total CXCR5 was scored for all cell types ( n = 50, 25 HPV+, 25 HPV−).** P = 0.0012, Student‘s 2 sided t test. Source data are provided as a Source Data file.

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    anti cxcr5  (Cell Signaling Technology Inc)


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    Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and <t>CXCR5</t> (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)
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    1) Product Images from "Enhanced humoral immunity in breast cancer patients with high serum concentration of anti‐HER2 autoantibody"

    Article Title: Enhanced humoral immunity in breast cancer patients with high serum concentration of anti‐HER2 autoantibody

    Journal: Cancer Medicine

    doi: 10.1002/cam4.3742

    Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and CXCR5 (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)
    Figure Legend Snippet: Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and CXCR5 (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)

    Techniques Used: Immunohistochemistry, MANN-WHITNEY

    anti cxcr5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti cxcr5
    Anti Cxcr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cxcr5 d6l3c  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cxcr5 d6l3c
    ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) <t>CXCR5</t> in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.
    Cxcr5 D6l3c, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "A highly potent lymphatic system–targeting nanoparticle cyclosporine prevents glomerulonephritis in mouse model of lupus"

    Article Title: A highly potent lymphatic system–targeting nanoparticle cyclosporine prevents glomerulonephritis in mouse model of lupus

    Journal: Science Advances

    doi: 10.1126/sciadv.abb3900

    ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) CXCR5 in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.
    Figure Legend Snippet: ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) CXCR5 in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.

    Techniques Used: Expressing

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    Cell Signaling Technology Inc rabbit anti cxcr5
    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and <t>CXCR5</t> (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.
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    TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers <t>(CXCR5</t> and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas
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    Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or <t>CXCR5</t> −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type
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    Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and <t>CXCR5</t> (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)
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    Cell Signaling Technology Inc cxcr5 d6l3c
    ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) <t>CXCR5</t> in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.
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    Image Search Results


    mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.

    Journal: Frontiers in Genetics

    Article Title: Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury

    doi: 10.3389/fgene.2022.946524

    Figure Lengend Snippet: mRNA and protein expression of key genes and related receptors. (A) mRNA expression of CCL21, XCR1, CXCL13, CASR, and EDN1. (B) Protein expression of CCL21, CXCL13, and XCR1. (C) Protein expression of GPR174/CCR7 (the receptors of CCL21) and CXCR5 (the receptors of CXCL13). n = 3–6. * p < 0.05, ** p < 0.01 vs. the sham group. I/R, ischemia reperfusion.

    Article Snippet: The primary antibodies were as follows: goat anti-CCL21 (1:1000; R&D Systems, Minneapolis, MN), rabbit anti-XCR1 (1:1000; Novus Biologicals, Littleton, CO), goat anti-CXCL13 (1:1000; R&D Systems, Minneapolis, MN), goat anti-CCR7 (1:1000; Novus Biologicals, Littleton, CO), rabbit anti-GPR174 (1:1000; Biorbyt, Cambridge, United Kingdom), rabbit anti-CXCR5 (1:1000; Absin, Shanghai, China), and rabbit anti-β-tubulin (1:5000; Cell Signaling Technology, Beverly, MA).

    Techniques: Expressing

    Journal: iScience

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    doi: 10.1016/j.isci.2022.103883

    Figure Lengend Snippet:

    Article Snippet: Rabbit anti-CXCR5 monoclonal antibody (D6L3C) , CST , Cat#: 72172S.

    Techniques: Recombinant, Software

    TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers (CXCR5 and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas

    Journal: iScience

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    doi: 10.1016/j.isci.2022.103883

    Figure Lengend Snippet: TLS formation in MIA tumors (A) The schema of TLS formation. The first stage is B & T cell aggregation. The second stage is follicle formation with T-zone and B-zone. The third stage is ectopic germinal center formation with formation with follicular dendritic cell in light-zone. (B) Hierarchical clustering of Z score normalized gene expression of B cell infiltration markers (CD19 and CD20), follicle phenotype markers (CXCR5 and CXCL13), and lymphocyte homing signal markers (CCR7 and CCL19). Color of the top bar represents tumor (red) or adjacent normal (blue) tissue. Correlations between expression levels from these six TLS markers and immune cell abundance corrected by tumor purity are shown in the right bar. p Values are calculated using Spearman correlation; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA six-plex TLS panel staining. The merged-channel multispectral image was captured after 5-cycle TSA staining and DAPI counterstain, revealing a classic lymphoid structure residing in MIA stromal tissue. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, CD20: red, CD35: cyan. Tfh cells are highlighted with white arrows (lower right corner images). (D–G) Paired comparisons of CD20 + B cell density, CD4 + T cell density (E), CD35 + follicle dendritic cell density (F), and CD8 + T cell density (G) between non-follicle (Non-Fol) and TLS areas

    Article Snippet: Rabbit anti-CXCR5 monoclonal antibody (D6L3C) , CST , Cat#: 72172S.

    Techniques: Expressing, Staining

    Treg recruitment as potential mechanism of decreased CD8 + T cell infiltration in tertiary lymphoid structures (A) Comparison of immune suppressive cell infiltration estimated from XCELL between MIA tumor and adjacent normal tissues. p values are calculated using Mann-Whitney U test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (B) Plot of Tfr/Tfh marker ratio vs CD8 + T cell infiltration. FoxP3, PDCD1, and IL2RA are markers of Tfr cells, while BCL6, ICOS, and IL7R are markers of Tfh cells. See text. p values are calculated using Spearman correlation test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA 7-plex panel staining for Tfr and Tfh. Merged multispectral image was captured after 6-cycle TSA staining and DAPI counterstain and reveals a mature TLS architecture. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, FOXP3: red, BCL6: cyan and CD3: orange. Sub-populations of CD4 + T cells are highlighted by arrows (Tfr: red, Treg: purple, Th: green and Tfh: cyan). (D) Paired comparison of CD8 + T cell density between non-follicle (Non-Fol) and TLS areas. (E) Paired comparison of ratio of regulatory T cells to helper T cells between TLS and non-follicle areas. (F) Comparison of CD8 + T cell density between groups with high and low Tfr/Tfh ratio

    Journal: iScience

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    doi: 10.1016/j.isci.2022.103883

    Figure Lengend Snippet: Treg recruitment as potential mechanism of decreased CD8 + T cell infiltration in tertiary lymphoid structures (A) Comparison of immune suppressive cell infiltration estimated from XCELL between MIA tumor and adjacent normal tissues. p values are calculated using Mann-Whitney U test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (B) Plot of Tfr/Tfh marker ratio vs CD8 + T cell infiltration. FoxP3, PDCD1, and IL2RA are markers of Tfr cells, while BCL6, ICOS, and IL7R are markers of Tfh cells. See text. p values are calculated using Spearman correlation test; ∗∗∗p < 0.001; ∗∗p < 0.01; ∗p < 0.05; ns p > 0.05. (C) Typical observation field of MIA 7-plex panel staining for Tfr and Tfh. Merged multispectral image was captured after 6-cycle TSA staining and DAPI counterstain and reveals a mature TLS architecture. Single channels are shown for the area bounded by the white rectangle. Fake colors are assigned as DAPI: blue, CD8: yellow, CXCR5: pink, CD4: green, FOXP3: red, BCL6: cyan and CD3: orange. Sub-populations of CD4 + T cells are highlighted by arrows (Tfr: red, Treg: purple, Th: green and Tfh: cyan). (D) Paired comparison of CD8 + T cell density between non-follicle (Non-Fol) and TLS areas. (E) Paired comparison of ratio of regulatory T cells to helper T cells between TLS and non-follicle areas. (F) Comparison of CD8 + T cell density between groups with high and low Tfr/Tfh ratio

    Article Snippet: Rabbit anti-CXCR5 monoclonal antibody (D6L3C) , CST , Cat#: 72172S.

    Techniques: MANN-WHITNEY, Marker, Staining

    Journal: iScience

    Article Title: Tertiary lymphoid structure and decreased CD8 + T cell infiltration in minimally invasive adenocarcinoma

    doi: 10.1016/j.isci.2022.103883

    Figure Lengend Snippet:

    Article Snippet: Rabbit anti-CXCR5 monoclonal antibody (D6L3C) , CST , Cat#: 72172S.

    Techniques: Recombinant, Software

    Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or CXCR5 −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: Schematic illustration of the experimental design. a Timeline of WT mice that underwent sham surgery or CLP. b Timeline of WT or CXCR5 −/− mice that underwent sham surgery or CLP. c Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the p38MAPK inhibitor SB203580 or agonist P79350. d Timeline of LPS-treated microglial cells treated with CXCR5 siRNA with or without pretreatment with the autophagy inhibitor 3-MA or agonist rapamycin. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, LPS lipopolysaccharide, siRNA short interfering RNA, 3-MA 3-methyladenine, WT wild-type

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Ligation, Small Interfering RNA

    Cognitive deficits and up-regulation of CXCR5 in a mouse model of sepsis-associated encephalopathy. Adult male C57BL/6 J mice were subjected to sham surgery or CLP. a Escape latency time, b time spent in the target quadrant, and c number of crossings over the target quadrant in the Morris water maze beginning on day 14 after CLP. d Freezing time in the fear conditioning test on day 19 after CLP ( n = 16 per group). e, f Western blot and densitometry of hippocampal CXCR5 on days 3, 7 and 14 after CLP ( n = 4 per group). GAPDH was used as an internal control. g Double staining of CXCR5 with microglia marker Iba-1 in the hippocampus at 14 days after CLP. Arrows indicate double-stained cells. Magnification, 200 × . Scale bar, 100 μm. h Quantification of immunofluorescent cells co-staining positive for CXCR5 and Iba-1. * p < 0.05 vs. sham. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: Cognitive deficits and up-regulation of CXCR5 in a mouse model of sepsis-associated encephalopathy. Adult male C57BL/6 J mice were subjected to sham surgery or CLP. a Escape latency time, b time spent in the target quadrant, and c number of crossings over the target quadrant in the Morris water maze beginning on day 14 after CLP. d Freezing time in the fear conditioning test on day 19 after CLP ( n = 16 per group). e, f Western blot and densitometry of hippocampal CXCR5 on days 3, 7 and 14 after CLP ( n = 4 per group). GAPDH was used as an internal control. g Double staining of CXCR5 with microglia marker Iba-1 in the hippocampus at 14 days after CLP. Arrows indicate double-stained cells. Magnification, 200 × . Scale bar, 100 μm. h Quantification of immunofluorescent cells co-staining positive for CXCR5 and Iba-1. * p < 0.05 vs. sham. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Western Blot, Double Staining, Marker, Staining, Ligation, Binding Assay

    CXCR5 knockout ameliorated sepsis-induced cognitive dysfunction in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and b densitometry of hippocampal CXCR5 on day 14 after CLP. GAPDH was used as an internal control ( n = 4 per group). Mice were assessed in the Morris water maze on day 14 after CLP, followed by the fear conditioning test. c Escape latency time, d time spent in the target quadrant, and e number of crossings over the target quadrant in the Morris water maze. f Freezing time in the fear conditioning test ( n = 16 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, WT wild-type

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockout ameliorated sepsis-induced cognitive dysfunction in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and b densitometry of hippocampal CXCR5 on day 14 after CLP. GAPDH was used as an internal control ( n = 4 per group). Mice were assessed in the Morris water maze on day 14 after CLP, followed by the fear conditioning test. c Escape latency time, d time spent in the target quadrant, and e number of crossings over the target quadrant in the Morris water maze. f Freezing time in the fear conditioning test ( n = 16 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, WT wild-type

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Knock-Out, Western Blot, Ligation

    CXCR5 knockout restored hippocampal autophagy in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Representative transmission electron micrographs of the hippocampus show zoomed-in views (magnification, 5000 × ; Scale bar, 500 nm) of full image of a cell (magnification, 2000 × ; Scale bar, 2000 nm). Arrows indicate autophagosome. b Representative immunofluorescence micrographs showing LC3 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. c Quantification of immunofluorescent cells staining positive for LC3. d – h Western blot and densitometry of hippocampal LC3, beclin-1, Atg-5 and p62, and the ratio of LC3-II/LC3-I. GAPDH was used as an internal control ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Atg-5 autophagy-related gene-5, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3, WT wild-type

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockout restored hippocampal autophagy in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Representative transmission electron micrographs of the hippocampus show zoomed-in views (magnification, 5000 × ; Scale bar, 500 nm) of full image of a cell (magnification, 2000 × ; Scale bar, 2000 nm). Arrows indicate autophagosome. b Representative immunofluorescence micrographs showing LC3 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. c Quantification of immunofluorescent cells staining positive for LC3. d – h Western blot and densitometry of hippocampal LC3, beclin-1, Atg-5 and p62, and the ratio of LC3-II/LC3-I. GAPDH was used as an internal control ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Atg-5 autophagy-related gene-5, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3, WT wild-type

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Knock-Out, Transmission Assay, Immunofluorescence, Staining, Western Blot, Ligation

    CXCR5 knockout reversed the alteration in hippocampal microglial M1/M2 polarization in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and densitometry of hippocampal Iba-1 on day 14 after CLP. b Representative micrographs of immunohistochemistry for Iba-1 in the hippocampal CA1 and the number of Iba-1-positive cells. Magnification, 200 × . Scale bar, 100 μm. Representative immunofluorescence micrographs and quantitation ( n = 4 per group) after staining for c M1 marker iNOS and d M2 marker Arg-1 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Arg-1 arginase-1, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, Iba-1 ionized calcium binding adaptor molecule-1, iNOS inducible nitric oxide synthase, WT wild-type

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockout reversed the alteration in hippocampal microglial M1/M2 polarization in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a Western blot and densitometry of hippocampal Iba-1 on day 14 after CLP. b Representative micrographs of immunohistochemistry for Iba-1 in the hippocampal CA1 and the number of Iba-1-positive cells. Magnification, 200 × . Scale bar, 100 μm. Representative immunofluorescence micrographs and quantitation ( n = 4 per group) after staining for c M1 marker iNOS and d M2 marker Arg-1 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. Arg-1 arginase-1, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, Iba-1 ionized calcium binding adaptor molecule-1, iNOS inducible nitric oxide synthase, WT wild-type

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Knock-Out, Western Blot, Immunohistochemistry, Immunofluorescence, Quantitation Assay, Staining, Marker, Ligation, Binding Assay

    CXCR5 knockout decreased hippocampal p-p38MAPK, IL-1β and IL-6 levels in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a – d Western blot and densitometry of hippocampal p-p38MAPK, p38MAPK, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, p38MAPK mitogen-activated protein kinase, p-p38MAPK phosphorylated p38MAPK, WT wild-type

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockout decreased hippocampal p-p38MAPK, IL-1β and IL-6 levels in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5 −/− ) were subjected to sham surgery or CLP. a – d Western blot and densitometry of hippocampal p-p38MAPK, p38MAPK, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. WT + sham; # p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, p38MAPK mitogen-activated protein kinase, p-p38MAPK phosphorylated p38MAPK, WT wild-type

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Knock-Out, Western Blot, Ligation

    CXCR5 knockdown restored p38MAPK-dependent autophagy in LPS-treated microglial cultures. Microglial cells were treated with CXCR5 siRNA. a Western blot and densitometry of CXCR5 in microglia at 24 h after CXCR5 siRNA administration. $ p < 0.05 vs. cells treated without siRNAs. Microglial cells were treated with CXCR5 siRNA at 24 h before LPS treatment. Some cultures were also treated with p38MAPK inhibitor SB203580 or agonist P79350 at 1 h before siRNA administration. b Representative micrographs of immunohistochemistry for LC3 in microglia at 24 h after LPS treatment. Magnification, 200 × . Scale bar, 100 μm. c Calculation of LC3-positive area. d – h Western blot and densitometry of LC3, beclin-1, Atg-5 and p62, and the ratio LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. Atg-5 autophagy-related gene-5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockdown restored p38MAPK-dependent autophagy in LPS-treated microglial cultures. Microglial cells were treated with CXCR5 siRNA. a Western blot and densitometry of CXCR5 in microglia at 24 h after CXCR5 siRNA administration. $ p < 0.05 vs. cells treated without siRNAs. Microglial cells were treated with CXCR5 siRNA at 24 h before LPS treatment. Some cultures were also treated with p38MAPK inhibitor SB203580 or agonist P79350 at 1 h before siRNA administration. b Representative micrographs of immunohistochemistry for LC3 in microglia at 24 h after LPS treatment. Magnification, 200 × . Scale bar, 100 μm. c Calculation of LC3-positive area. d – h Western blot and densitometry of LC3, beclin-1, Atg-5 and p62, and the ratio LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. Atg-5 autophagy-related gene-5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Western Blot, Immunohistochemistry

    CXCR5 knockdown reversed the alteration of p38MAPK-dependent microglial M1/M2 polarization and production of inflammatory cytokines in LPS-treated microglial cultures. a Representative micrographs of immunohistochemistry for Iba-1 in the microglia. Magnification, 200 × . Scale bar, 100 μm. b Calculation of Iba-1-positive area. c – h Western blot and densitometry of Iba-1, CD86, CD206, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin-1β, IL-6 interleukin-6, LPS lipopolysaccharide

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockdown reversed the alteration of p38MAPK-dependent microglial M1/M2 polarization and production of inflammatory cytokines in LPS-treated microglial cultures. a Representative micrographs of immunohistochemistry for Iba-1 in the microglia. Magnification, 200 × . Scale bar, 100 μm. b Calculation of Iba-1-positive area. c – h Western blot and densitometry of Iba-1, CD86, CD206, IL-1β and IL-6 ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin-1β, IL-6 interleukin-6, LPS lipopolysaccharide

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Immunohistochemistry, Western Blot, Binding Assay

    CXCR5 knockdown inhibited activation of p38MAPK-dependent NF-κB/STAT3 signaling in LPS-treated microglial cultures. a – d Western blot and densitometry of p-p38MAPK, p38MAPK, p-NF-κB, NF-κB, p-STAT3 and STAT3 and relevant ratios ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK p38 mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: CXCR5 knockdown inhibited activation of p38MAPK-dependent NF-κB/STAT3 signaling in LPS-treated microglial cultures. a – d Western blot and densitometry of p-p38MAPK, p38MAPK, p-NF-κB, NF-κB, p-STAT3 and STAT3 and relevant ratios ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. GAPDH glyceraldehyde-3-phosphate dehydrogenase, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK p38 mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Activation Assay, Western Blot

    Autophagy inhibition attenuated the effects of CXCR5 knockdown on microglial polarization and inflammatory cytokines production in LPS-treated microglial cultures. a – g Western blot and densitometry of LC3, Iba-1, CD86, and CD206, IL-1β, IL-6 and the ratio of LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, 3-MA 3-methyladenine

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: Autophagy inhibition attenuated the effects of CXCR5 knockdown on microglial polarization and inflammatory cytokines production in LPS-treated microglial cultures. a – g Western blot and densitometry of LC3, Iba-1, CD86, and CD206, IL-1β, IL-6 and the ratio of LC3-II/LC3-I ( n = 4 per group). * p < 0.05 vs. control; # p < 0.05 vs. LPS; & P < 0.05 vs. LPS + CXCR5 siRNA. CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1, IL-1β interleukin (IL)-1β, IL-6 interleukin (IL)-6, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, 3-MA 3-methyladenine

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Inhibition, Western Blot, Binding Assay

    Schematic diagram depicting the possible mechanisms through which CXCR5 regulates autophagy. MAPK signaling downstream of CXCR5 induced by LPS promotes the up-regulation of NF-κB/STAT3 axis. Consequently, activation of NF-κB/STAT3 pathway contributes to incomplete activation of autophagy and production of inflammatory cytokines, thereby impairs learning and memory function. CXCR5 down-regulation results in inhibition of MAPK/NF-κB/STAT3 axis and activation of autophagy in brain, which leads to the improved cognitive function in mice with sepsis-associated encephalopathy. Atg-5 autophagy-related gene-5, CXCR5 C-X-C chemokine receptor type 5, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Journal: Journal of Neuroinflammation

    Article Title: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

    doi: 10.1186/s12974-021-02300-1

    Figure Lengend Snippet: Schematic diagram depicting the possible mechanisms through which CXCR5 regulates autophagy. MAPK signaling downstream of CXCR5 induced by LPS promotes the up-regulation of NF-κB/STAT3 axis. Consequently, activation of NF-κB/STAT3 pathway contributes to incomplete activation of autophagy and production of inflammatory cytokines, thereby impairs learning and memory function. CXCR5 down-regulation results in inhibition of MAPK/NF-κB/STAT3 axis and activation of autophagy in brain, which leads to the improved cognitive function in mice with sepsis-associated encephalopathy. Atg-5 autophagy-related gene-5, CXCR5 C-X-C chemokine receptor type 5, LC3 microtubule-associated protein 1 light chain 3, LPS lipopolysaccharide, NF-κB nuclear factor kappa-B, p38MAPK mitogen-activated protein kinase, p- phosphorylated, STAT3 signal transducer and activator of transcription

    Article Snippet: For co-labeling of CXCR5 and Iba-1, sections were incubated overnight at 4 °C with primary antibodies (Invitrogen) against CXCR5 (1:300) and Iba-1 (1:300), then incubated with an anti-mouse or anti-rabbit IgG (1:1000; Cell Signaling Technology) conjugated with Alexa Fluor® 488 and Alexa Fluor® 594.

    Techniques: Activation Assay, Inhibition

    Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and CXCR5 (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)

    Journal: Cancer Medicine

    Article Title: Enhanced humoral immunity in breast cancer patients with high serum concentration of anti‐HER2 autoantibody

    doi: 10.1002/cam4.3742

    Figure Lengend Snippet: Tumor‐infiltrating CD20‐positive ICs, IGKC‐positive ICs, and CXCL13‐positive ICs, and follicular CD4‐positive ICs in the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. (A–F) Representative photographs of IHC staining for CD20 (A and B), IGKC (C and D), and CXCL13 (E and F) of the tumors with large cell counts (A, C and E) and the tumors with small cell counts (B, D and F). (G–J) Representative photographs of IHC staining for CD4 (brown) and CXCR5 (red) of the regional axillary lymph nodes with large cell counts (G and I) and with small cell counts (H and J). Images (I) and (J) are the high power fields of the images (G) and (H), respectively. Original magnification, ×20 (A–H) and ×40 (I and J). (K–M) Counts of ICs positive for CD20 (K), IGKC (L), and CXCL13 (M) in the high HER2‐AAb group and the low HER2‐AAb group. (N) Counts of CD4‐positive ICs in CXCR5‐positive B‐cell follicles (follicular CD4 + ) of the regional axillary lymph nodes in the high HER2‐AAb group and the low HER2‐AAb group. Medians are shown by horizontal dotted lines. p , Mann–Whitney U test. Scale bar, 100 µm (A–H) and 50 µm (I and J)

    Article Snippet: The following primary antibodies were used: polyclonal anti‐Kappa Light Chain (1:200, Invitrogen), anti‐CD20 (L26, 1:50, Abcam), anti‐HLA Class 1 ABC (EMR8‐5, 1:100, Abcam), anti‐CD8 (C8/144B, 1:100, Dako), anti‐FOXP3 (236A/E7, 1:100, Abcam), anti‐CXCR5 (D6L3C, 1:200, Cell Signaling Technology), anti‐CD4 (4B12, 1:80, Dako), polyclonal anti‐CXCL13 (1:100, Invitrogen), and SP142‐compatible anti‐PD‐L1 (28‐8, 1:400, Abcam).

    Techniques: Immunohistochemistry, MANN-WHITNEY

    ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) CXCR5 in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.

    Journal: Science Advances

    Article Title: A highly potent lymphatic system–targeting nanoparticle cyclosporine prevents glomerulonephritis in mouse model of lupus

    doi: 10.1126/sciadv.abb3900

    Figure Lengend Snippet: ( A ) Histological images showing that renal damage in the untreated MRL- lpr appeared to have a strong correlation with lymphocyte infiltration. Both CD20 + and CD3 + cells were enriched in the glomeruli (CD20 and CD3) and the interstitial space (CD3) ( n = 15 to 30 micrographs from at least three individuals; scale bars, 50 μm for first two rows of images; scale bars, 200 μm for third row of images). ( B ) Graphical analyses of CD20 + cells and ( C ) CD3 + cells in the histological images. ( D ) We observed elevated transcript levels of CXCR4 and ( E ) CXCR5 in the untreated MRL- lpr mice ( n = 5 to 6 individuals). ( F ) Renal histology also showed significant up-regulation of CXCR4 (brown) among infiltrating leukocytes and endogenous expression in the proximal tubules. CXCR5 + population (red) appeared to decorate the migrating front of infiltrating leukocytes. (scale bars, 200 μm for all images). Representative micrographs are shown. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001. Statistics were conducted against the MRL- lpr group. Comparisons were made with one-way ANOVA, followed by Tukey’s multiple comparisons test.

    Article Snippet: Immunohistochemistry and immunofluorescence antibodies for CD20 (polyclonal) and IgG (polyclonal, Alexa Fluor 488) were purchased from Thermo Fisher Scientific (Waltham, MA); antibodies for WT1 (D8175), CXCR4 (D4Z7W), and CXCR5 (D6L3C) were purchased from Cell Signaling Technology (Danvers, MA); antibody for CD3 (polyclonal) was purchased from Agilent (Santa Clara, CA); and antibody for nephrin (polyclonal) was purchased from R&D Systems (Minneapolis, MN).

    Techniques: Expressing