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Novus Biologicals immunofluorescence
Immunofluorescence, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nur77/NGFI-B+alpha%2FNur77%2FNR4A1+Antibody/pmc13131444-179-6-9
Average 94 stars, based on 23 article reviews

immunofluorescence - by Bioz Stars, 2026-10

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Article Title: Targeting KPNB1 with genkwadaphnin suppresses gastric cancer progression through the Nur77-mediated signaling pathway.
Article Snippet: Gastric cancer (GC) remains a global challenge due to the lack of early detection and precision therapies.. Genkwadaphnin (DD1), a natural diterpene isolated from the bud of Flos GenkWa (Thymelaeaceae), serves as a Karyopherin β1 (KPNB1) inhibitor.. In this study, we investigated the anti-tumor effect of DD1 in both cell culture and animal models.

Blocking Assay:

Article Title: Single-cell RNA-Seq analysis of molecular changes during radiation-induced skin injury: the involvement of Nur77
Article Snippet: .. Cells were blocked with blocking buffer (phosphate buffered saline, 1% Triton X-100, and 5% BSA) and incubated at 4 °C with Nur77 (#NBP2-66980, Novus) antibody (1: 200) overnight, FITC-conjugated goat anti-mouse antibody (1:300) was added for 2 h at room temperature, and cells were dyed with 200 nM MitoTracker Red CMXRos (#C1035, Beyotime) at 37 °C for 30 min in darkness. .. Nuclei were counterstained with DAPI (#P0131, Beyotime).

Saline:

Incubation:

Image Search Results

( A ) Identification of Nur77 arginine methylation sites. Top: Western blot analysis of SDMA-modified Nur77 in HEK293T cells; bottom: Evolutionary conservation of Nur77 R346 across vertebrate species. ( B ) In vitro methylation analysis of PRMT5 on Nur77 wild-type and various domain mutants. ( C ) Dot blot validation experiment of Nur77-R346me2s–specific antibody, using different antibody concentrations (111, 37, 12 ng/mL) to detect specific binding to various methylated peptides. ( D ) Western blot detection of intracellular Nur77 methylation status following overexpression of wild-type Nur77 and R346K mutant. ( E and F ) RT-qPCR analysis of decidualization markers PRL ( E ) and IGFBP1 ( F ) mRNA expression levels in Nur77 knockdown and wild-type or R346K mutant rescue experiments ( n = 3). ( G – L ) Effects of PRMT5 overexpression on decidualization in Nur77-knockdown EnSCs rescued with wild-type or R346K mutant Nur77: Western blot analysis of PRMT5, Nur77, and Nur77-R346me2s ( G ); RT-qPCR analysis of PRL ( H ) and IGFBP1 ( I ) mRNA levels; immunofluorescence analysis of F-actin cytoskeletal remodeling ( J ); trophoblast spheroid invasion assay ( K and L ). Data represent mean ± SEM. ** P < 0.01; *** P < 0.001; **** P < 0.0001; 1-way ANOVA with Tukey’s multiple comparisons test in ( E , F , H , I , and L ). Scale bar: 100 μm. NT, N-terminal domain; DBD, DNA-binding domain; LBD, ligand-binding domain.

Journal: The Journal of Clinical Investigation

Article Title: Targeting the PRMT5/Nur77 methylation axis enhances endometrial decidualization capacity and female fertility in preclinical models

doi: 10.1172/JCI178862

Figure Lengend Snippet: ( A ) Identification of Nur77 arginine methylation sites. Top: Western blot analysis of SDMA-modified Nur77 in HEK293T cells; bottom: Evolutionary conservation of Nur77 R346 across vertebrate species. ( B ) In vitro methylation analysis of PRMT5 on Nur77 wild-type and various domain mutants. ( C ) Dot blot validation experiment of Nur77-R346me2s–specific antibody, using different antibody concentrations (111, 37, 12 ng/mL) to detect specific binding to various methylated peptides. ( D ) Western blot detection of intracellular Nur77 methylation status following overexpression of wild-type Nur77 and R346K mutant. ( E and F ) RT-qPCR analysis of decidualization markers PRL ( E ) and IGFBP1 ( F ) mRNA expression levels in Nur77 knockdown and wild-type or R346K mutant rescue experiments ( n = 3). ( G – L ) Effects of PRMT5 overexpression on decidualization in Nur77-knockdown EnSCs rescued with wild-type or R346K mutant Nur77: Western blot analysis of PRMT5, Nur77, and Nur77-R346me2s ( G ); RT-qPCR analysis of PRL ( H ) and IGFBP1 ( I ) mRNA levels; immunofluorescence analysis of F-actin cytoskeletal remodeling ( J ); trophoblast spheroid invasion assay ( K and L ). Data represent mean ± SEM. ** P < 0.01; *** P < 0.001; **** P < 0.0001; 1-way ANOVA with Tukey’s multiple comparisons test in ( E , F , H , I , and L ). Scale bar: 100 μm. NT, N-terminal domain; DBD, DNA-binding domain; LBD, ligand-binding domain.

Article Snippet: Anti–Nur77-R346me2s rabbit polyclonal antibody was generated by ABclonal.

Techniques: Methylation, Western Blot, Modification, In Vitro, Dot Blot, Biomarker Discovery, Binding Assay, Over Expression, Mutagenesis, Quantitative RT-PCR, Expressing, Knockdown, Immunofluorescence, Invasion Assay, Ligand Binding Assay

( A ) Representative fluorescence images showing the intracellular uptake of FITC-labeled wild-type (FITC-Pep-Nur77 WT ) and mutant (FITC-Pep-Nur77 R346K ) peptides in human EnSCs. ( B and C ) RT-qPCR analysis of decidualization markers IGFBP1 ( B ) and PRL ( C ) mRNA expression levels in EnSCs treated with control vehicle, Pep-Nur77 WT , or Pep-Nur77 R346K under decidualization conditions (MPA+cAMP). ( D ) Top: Schematic representation of the amino acid sequences of cell-permeable peptides containing the TAT transduction domain. Bottom: Domain structure of Nur77 highlighting the conserved R346 site and phosphorylation sites S341/S351. ( E ) Molecular docking simulation showing the interaction interfaces of AKT and PRMT5 with Pep-Nur77 WT and Pep-Nur77 R346K . ( F ) Co-immunoprecipitation analysis of endogenous Nur77 interactions with PRMT5 and AKT following treatment with Nur77-derived peptides. ( G ) Western blot analysis of temporal changes in Nur77 methylation (R346me2s) and phosphorylation (S341, S351) during the decidualization process (0–72 hours). ( H – L ) Functional rescue of PRMT5-depleted EnSCs with Pep-Nur77 R346K : RT-qPCR analysis of IGFBP1 ( H ) and PRL ( I ) mRNA levels; Western blot analysis of PRMT5, Nur77-R346me2s, pNur77-S341, and pNur77-S351 status ( J ). ( K and L ) Trophoblast spheroid invasion assay with representative images ( K ) and quantification ( L ). Data represent mean ± SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; 1-way ANOVA with Tukey’s multiple comparisons test ( B , C , H , I , and L ). White scale bar: 50 μm.

Journal: The Journal of Clinical Investigation

Article Title: Targeting the PRMT5/Nur77 methylation axis enhances endometrial decidualization capacity and female fertility in preclinical models

doi: 10.1172/JCI178862

Figure Lengend Snippet: ( A ) Representative fluorescence images showing the intracellular uptake of FITC-labeled wild-type (FITC-Pep-Nur77 WT ) and mutant (FITC-Pep-Nur77 R346K ) peptides in human EnSCs. ( B and C ) RT-qPCR analysis of decidualization markers IGFBP1 ( B ) and PRL ( C ) mRNA expression levels in EnSCs treated with control vehicle, Pep-Nur77 WT , or Pep-Nur77 R346K under decidualization conditions (MPA+cAMP). ( D ) Top: Schematic representation of the amino acid sequences of cell-permeable peptides containing the TAT transduction domain. Bottom: Domain structure of Nur77 highlighting the conserved R346 site and phosphorylation sites S341/S351. ( E ) Molecular docking simulation showing the interaction interfaces of AKT and PRMT5 with Pep-Nur77 WT and Pep-Nur77 R346K . ( F ) Co-immunoprecipitation analysis of endogenous Nur77 interactions with PRMT5 and AKT following treatment with Nur77-derived peptides. ( G ) Western blot analysis of temporal changes in Nur77 methylation (R346me2s) and phosphorylation (S341, S351) during the decidualization process (0–72 hours). ( H – L ) Functional rescue of PRMT5-depleted EnSCs with Pep-Nur77 R346K : RT-qPCR analysis of IGFBP1 ( H ) and PRL ( I ) mRNA levels; Western blot analysis of PRMT5, Nur77-R346me2s, pNur77-S341, and pNur77-S351 status ( J ). ( K and L ) Trophoblast spheroid invasion assay with representative images ( K ) and quantification ( L ). Data represent mean ± SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; 1-way ANOVA with Tukey’s multiple comparisons test ( B , C , H , I , and L ). White scale bar: 50 μm.

Article Snippet: Anti–Nur77-R346me2s rabbit polyclonal antibody was generated by ABclonal.

Techniques: Fluorescence, Labeling, Mutagenesis, Quantitative RT-PCR, Expressing, Control, Transduction, Phospho-proteomics, Immunoprecipitation, Derivative Assay, Western Blot, Methylation, Functional Assay, Invasion Assay

( A ) Effects of Pep-Nur77 R346K intrauterine perfusion on implantation site numbers ( n = 3) on D6 in Prmt5 d/d mice. ( B ) Western blot analysis of PRMT5, Nur77, Nur77-R346me2s, and pNur77 (S351) levels in endometrial tissues of Prmt5 d/d mice treated with Pep-Nur77 R346K . ( C and D ) Effects of Pep-Nur77 R346K on artificial decidualization in Prmt5 d/d mice: schematic of the experimental schedule ( C ); gross uterine morphology and weight ratio analysis of decidualized (oil-stimulated) to control sides ( D ). ( E – H ) Effects of Pep-Nur77 R346K on GSK591-induced implantation failure: schematic of the experimental design ( E ); representative uterine images and quantification of implantation sites on D8 ( F ); immunofluorescence analysis of the decidual marker DTPRP ( G ); Western blot analysis of uterine PRMT5 and Nur77 modification status ( H ). ( I and J ) Effects of Pep-Nur77 R346K on artificial decidualization in GSK591-treated mice, showing gross morphology and decidual weight ratio. Data represent mean ± SEM. ** P < 0.01; **** P < 0.0001; Student’s t test ( A and D ); 1-way ANOVA with Tukey’s multiple comparisons test ( F and J ). Scale bar: 100 μm.

Journal: The Journal of Clinical Investigation

Article Title: Targeting the PRMT5/Nur77 methylation axis enhances endometrial decidualization capacity and female fertility in preclinical models

doi: 10.1172/JCI178862

Figure Lengend Snippet: ( A ) Effects of Pep-Nur77 R346K intrauterine perfusion on implantation site numbers ( n = 3) on D6 in Prmt5 d/d mice. ( B ) Western blot analysis of PRMT5, Nur77, Nur77-R346me2s, and pNur77 (S351) levels in endometrial tissues of Prmt5 d/d mice treated with Pep-Nur77 R346K . ( C and D ) Effects of Pep-Nur77 R346K on artificial decidualization in Prmt5 d/d mice: schematic of the experimental schedule ( C ); gross uterine morphology and weight ratio analysis of decidualized (oil-stimulated) to control sides ( D ). ( E – H ) Effects of Pep-Nur77 R346K on GSK591-induced implantation failure: schematic of the experimental design ( E ); representative uterine images and quantification of implantation sites on D8 ( F ); immunofluorescence analysis of the decidual marker DTPRP ( G ); Western blot analysis of uterine PRMT5 and Nur77 modification status ( H ). ( I and J ) Effects of Pep-Nur77 R346K on artificial decidualization in GSK591-treated mice, showing gross morphology and decidual weight ratio. Data represent mean ± SEM. ** P < 0.01; **** P < 0.0001; Student’s t test ( A and D ); 1-way ANOVA with Tukey’s multiple comparisons test ( F and J ). Scale bar: 100 μm.

Article Snippet: Anti–Nur77-R346me2s rabbit polyclonal antibody was generated by ABclonal.

Techniques: Western Blot, Control, Immunofluorescence, Marker, Modification

( A ) Representative immunofluorescence images of PRMT5 (green), Nur77-R346me2s (red), and total Nur77 (cyan) in endometrial sections from FER and RIF patients. Nuclei were stained with DAPI (gray). ( B ) Representative Western blot image of PRMT5 and Nur77 methylation modification levels in endometria from FER and RIF patients. ( C – E ) Semiquantitative analysis of protein expression of ( C ) PRMT5, ( D ) total Nur77, and ( E ) Nur77-R346me2s in control ( n = 39) and RIF ( n = 75) endometrial tissues. ( F ) Correlation analysis between PRMT5 protein levels and Nur77-R346me2s intensity in human endometrial tissues. ( G ) Flowchart illustrating the inclusion and exclusion criteria for the clinical study participation and analysis. ( H ) ROC curve analysis of clinical variables alone and clinical variables plus Nur77-R346me2s. Data represent mean ± SEM. **** P < 0.0001. Student’s t test ( C – E ). Scale bar: 100 μm.

Journal: The Journal of Clinical Investigation

Article Title: Targeting the PRMT5/Nur77 methylation axis enhances endometrial decidualization capacity and female fertility in preclinical models

doi: 10.1172/JCI178862

Figure Lengend Snippet: ( A ) Representative immunofluorescence images of PRMT5 (green), Nur77-R346me2s (red), and total Nur77 (cyan) in endometrial sections from FER and RIF patients. Nuclei were stained with DAPI (gray). ( B ) Representative Western blot image of PRMT5 and Nur77 methylation modification levels in endometria from FER and RIF patients. ( C – E ) Semiquantitative analysis of protein expression of ( C ) PRMT5, ( D ) total Nur77, and ( E ) Nur77-R346me2s in control ( n = 39) and RIF ( n = 75) endometrial tissues. ( F ) Correlation analysis between PRMT5 protein levels and Nur77-R346me2s intensity in human endometrial tissues. ( G ) Flowchart illustrating the inclusion and exclusion criteria for the clinical study participation and analysis. ( H ) ROC curve analysis of clinical variables alone and clinical variables plus Nur77-R346me2s. Data represent mean ± SEM. **** P < 0.0001. Student’s t test ( C – E ). Scale bar: 100 μm.

Article Snippet: Anti–Nur77-R346me2s rabbit polyclonal antibody was generated by ABclonal.

Techniques: Immunofluorescence, Staining, Western Blot, Methylation, Modification, Expressing, Control

Thermoneutrality augments TCR signaling strength (A–J) 8-to-10-week-old Nur77 GFP C57BL/6J male mice were housed in Tn (30 °C)- or Ts (22 °C)-conditions. After 2 weeks, splenic T cells (CD45 + TCRβ + TCRγδ − NK1.1 - ) were characterized via flow cytometry (n = 4–10 biological replicates per group). (A) Schematic overview. (B) Representative flow cytometric plot of Nur77-GFP expression in splenic CD4 + (left) and CD8 + (right) T cells. (C, D) Frequency of Nur77-GFP + CD4 + T cells (C) and CD8 + T cells (D). (E, F) Relative mean fluorescence intensity (MFI) of Nur77-GFP in CD4 + T cells (E) and CD8 + T cells (F). (G, H) Relative MFI of CD69 in CD4 + T cells (G) and CD8 + T cells (H). (I, J) Frequency of CD5 hi Ly6C − CD4 + T cells (I) and CD8 + T cells (J). (K, L) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn (30 °C)- or Ts (22 °C)-conditions. After 2 weeks, splenic CD4 + T cells were negatively selected via magnetic separation and stimulated ex vivo with anti-CD3 and anti-CD28 for the indicated times. Levels of phosphorylated ZAP70 (p-ZAP70) and total ZAP70 were quantified via western blot analysis ( n = 4 biological replicates per group). (K) Representative western blot. (L) Quantification of relative phosphorylated-to-total ZAP70 ratio. Statistical analysis was performed between each time point, in addition to the total area under the curve (AUC), for each group. (E-H) MFI of each data point was divided by the average MFI in the control (Ts-housed) group per experiment to yield relative MFI. (L) Relative phospho-to-total ZAP70 ratios of each timepoint were normalized to that of the 0 min timepoint of the Ts replicate per membrane. (C-L) Mann-Whitney U test. ∗: p < 0.05, ∗∗: p < 0.01, and ∗∗∗: p < 0.001 (Ts vs. Tn). #: p < 0.05 (Ts AUC vs. Tn AUC). For bar graphs, data represent mean ± SEM. For the line graph, data represent mean ± SEM, and the shaded region under the lines represents the area used to calculate AUC.

Journal: iScience

Article Title: Ambient temperature regulates CD4 + T cell tonic T cell receptor signaling and responsiveness

doi: 10.1016/j.isci.2026.115801

Figure Lengend Snippet: Thermoneutrality augments TCR signaling strength (A–J) 8-to-10-week-old Nur77 GFP C57BL/6J male mice were housed in Tn (30 °C)- or Ts (22 °C)-conditions. After 2 weeks, splenic T cells (CD45 + TCRβ + TCRγδ − NK1.1 - ) were characterized via flow cytometry (n = 4–10 biological replicates per group). (A) Schematic overview. (B) Representative flow cytometric plot of Nur77-GFP expression in splenic CD4 + (left) and CD8 + (right) T cells. (C, D) Frequency of Nur77-GFP + CD4 + T cells (C) and CD8 + T cells (D). (E, F) Relative mean fluorescence intensity (MFI) of Nur77-GFP in CD4 + T cells (E) and CD8 + T cells (F). (G, H) Relative MFI of CD69 in CD4 + T cells (G) and CD8 + T cells (H). (I, J) Frequency of CD5 hi Ly6C − CD4 + T cells (I) and CD8 + T cells (J). (K, L) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn (30 °C)- or Ts (22 °C)-conditions. After 2 weeks, splenic CD4 + T cells were negatively selected via magnetic separation and stimulated ex vivo with anti-CD3 and anti-CD28 for the indicated times. Levels of phosphorylated ZAP70 (p-ZAP70) and total ZAP70 were quantified via western blot analysis ( n = 4 biological replicates per group). (K) Representative western blot. (L) Quantification of relative phosphorylated-to-total ZAP70 ratio. Statistical analysis was performed between each time point, in addition to the total area under the curve (AUC), for each group. (E-H) MFI of each data point was divided by the average MFI in the control (Ts-housed) group per experiment to yield relative MFI. (L) Relative phospho-to-total ZAP70 ratios of each timepoint were normalized to that of the 0 min timepoint of the Ts replicate per membrane. (C-L) Mann-Whitney U test. ∗: p < 0.05, ∗∗: p < 0.01, and ∗∗∗: p < 0.001 (Ts vs. Tn). #: p < 0.05 (Ts AUC vs. Tn AUC). For bar graphs, data represent mean ± SEM. For the line graph, data represent mean ± SEM, and the shaded region under the lines represents the area used to calculate AUC.

Article Snippet: Nur77 GFP mice , Jackson Laboratory , Strain #: 016617; RRID: IMSR_JAX:016617.

Techniques: Flow Cytometry, Expressing, Fluorescence, Ex Vivo, Western Blot, Control, Membrane, MANN-WHITNEY

Thermoneutrality alters CD4 + T cell transcriptome upon tonic TCR signaling activation 8-to-10-week-old Nur77 GFP C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic Nur77-GFP + and Nur77-GFP - CD4 + T cells (CD45 + TCRβ + TCRγδ − NK1.1 − CD4 + ) from each condition were isolated via fluorescence-activated cell sorting. Transcriptomic analysis was then performed via bulk RNA-sequencing (n = 3–4 biological replicates per group). (A) Schematic overview. (B) Principal component analysis. Orange: Nur77-GFP - CD4 + T cells from Tn-housed mice. Red: Nur77-GFP + CD4 + T cells from Tn-housed mice. Light blue: Nur77-GFP - CD4 + T cells from Ts-housed mice. Dark blue: Nur77-GFP + CD4 + T cells from Ts-housed mice. Ovals represent a visual enclosing shape. (C) Volcano plot of gene expression levels between Nur77-GFP + CD4 + T cells from Tn- or Ts-housed mice. Red dots represent genes significantly upregulated (FC > 1.5, p -value <0.05) in Tn-housed mice. Blue dots represent genes significantly upregulated (FC < −1.5, p -value <0.05) in Ts-housed mice. (D) ToppGene functional enrichment analysis of genes significantly upregulated in Ts-housed mice. (E) ToppGene functional enrichment analysis of genes significantly upregulated in Tn-housed mice.

Journal: iScience

Article Title: Ambient temperature regulates CD4 + T cell tonic T cell receptor signaling and responsiveness

doi: 10.1016/j.isci.2026.115801

Figure Lengend Snippet: Thermoneutrality alters CD4 + T cell transcriptome upon tonic TCR signaling activation 8-to-10-week-old Nur77 GFP C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic Nur77-GFP + and Nur77-GFP - CD4 + T cells (CD45 + TCRβ + TCRγδ − NK1.1 − CD4 + ) from each condition were isolated via fluorescence-activated cell sorting. Transcriptomic analysis was then performed via bulk RNA-sequencing (n = 3–4 biological replicates per group). (A) Schematic overview. (B) Principal component analysis. Orange: Nur77-GFP - CD4 + T cells from Tn-housed mice. Red: Nur77-GFP + CD4 + T cells from Tn-housed mice. Light blue: Nur77-GFP - CD4 + T cells from Ts-housed mice. Dark blue: Nur77-GFP + CD4 + T cells from Ts-housed mice. Ovals represent a visual enclosing shape. (C) Volcano plot of gene expression levels between Nur77-GFP + CD4 + T cells from Tn- or Ts-housed mice. Red dots represent genes significantly upregulated (FC > 1.5, p -value <0.05) in Tn-housed mice. Blue dots represent genes significantly upregulated (FC < −1.5, p -value <0.05) in Ts-housed mice. (D) ToppGene functional enrichment analysis of genes significantly upregulated in Ts-housed mice. (E) ToppGene functional enrichment analysis of genes significantly upregulated in Tn-housed mice.

Article Snippet: Nur77 GFP mice , Jackson Laboratory , Strain #: 016617; RRID: IMSR_JAX:016617.

Techniques: Activation Assay, Isolation, Fluorescence, FACS, RNA Sequencing, Gene Expression, Functional Assay

Thermoneutrality-driven augmentation of CD4 + T cell TCR signaling strength is mediated by MHC class II presentation of self-peptide (A and B) 8-to-10-week-old OT-II transgenic (Tg) C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic CD4 + T cells (CD45 + TCRβ + TCRγδ − NK1.1 − CD4 + ) were characterized via flow cytometry (n = 5–9 biological replicates per group). (A) Schematic overview. (B) Relative MFI of Nur77. (C–F) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn- or Ts-conditions. Mice were treated with anti-MHCII antibodies (250 μg/mouse) or saline control via intraperitoneal injections every three days for 2 weeks. After 2 weeks, splenic immune cells (CD45 + ) were characterized via flow cytometry ( n = 3 biological replicates per group). (C) Schematic overview. (D) Cell counts of MHCII + B cells (B220 + CD11c − ). (E) Cell counts of MHCII + dendritic cells (DCs; CD11c + ). (F) Relative MFI of Nur77 in CD4 + T cells. (G and H) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic immune cells (CD45 + ) were characterized via flow cytometry ( n = 3 biological replicates per group). Relative MFI of CD80 and CD86 in B cells (G) and DCs (H). (B, F-H) MFI of each data point was divided by the average MFI in the control (Ts-housed) group per experiment to yield relative MFI. (B, D-F) Permutation test with Bonferroni correction for multiple comparisons. (G-H) Mann-Whitney U test. ∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001. For bar graphs, data represent mean ± SEM.

Journal: iScience

Article Title: Ambient temperature regulates CD4 + T cell tonic T cell receptor signaling and responsiveness

doi: 10.1016/j.isci.2026.115801

Figure Lengend Snippet: Thermoneutrality-driven augmentation of CD4 + T cell TCR signaling strength is mediated by MHC class II presentation of self-peptide (A and B) 8-to-10-week-old OT-II transgenic (Tg) C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic CD4 + T cells (CD45 + TCRβ + TCRγδ − NK1.1 − CD4 + ) were characterized via flow cytometry (n = 5–9 biological replicates per group). (A) Schematic overview. (B) Relative MFI of Nur77. (C–F) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn- or Ts-conditions. Mice were treated with anti-MHCII antibodies (250 μg/mouse) or saline control via intraperitoneal injections every three days for 2 weeks. After 2 weeks, splenic immune cells (CD45 + ) were characterized via flow cytometry ( n = 3 biological replicates per group). (C) Schematic overview. (D) Cell counts of MHCII + B cells (B220 + CD11c − ). (E) Cell counts of MHCII + dendritic cells (DCs; CD11c + ). (F) Relative MFI of Nur77 in CD4 + T cells. (G and H) 8-to-10-week-old WT C57BL/6J male mice were housed in Tn- or Ts-conditions. After 2 weeks, splenic immune cells (CD45 + ) were characterized via flow cytometry ( n = 3 biological replicates per group). Relative MFI of CD80 and CD86 in B cells (G) and DCs (H). (B, F-H) MFI of each data point was divided by the average MFI in the control (Ts-housed) group per experiment to yield relative MFI. (B, D-F) Permutation test with Bonferroni correction for multiple comparisons. (G-H) Mann-Whitney U test. ∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001. For bar graphs, data represent mean ± SEM.

Article Snippet: Nur77 GFP mice , Jackson Laboratory , Strain #: 016617; RRID: IMSR_JAX:016617.

Techniques: Transgenic Assay, Flow Cytometry, Saline, Control, MANN-WHITNEY

Effects of H 2 S on NR4A1-mediated intrinsic apoptosis of tumor cells with different expression level of IDO1. Cells were treated with NaHS (2 mM) or GYY4137 (400 μM) for 24 h. A , B Mitochondria in IDO1 knockdown MCF-7 cells detected by fluorescence staining. Magnification: 400×; scale bars represent 50 μm. C CF488-labeled Cyt C (green) in MCF-7 cells upon different treatments recorded by fluorescence microscopy. DAPI (blue) was used for nuclear staining. Representative image of three independent experiments is shown. Scale bars represent 10 μm. D Protein expressions of IDO1, BCL-2, and BAX in IDO1 knockdown MCF-7 cells and IDO1-overexpressing A549 cells detected by WB. Statistical plots are shown in Supplementary Fig. S2. E – G Apoptosis of NR4A1 knockdown MCF-7, SGC-7901, or A549 cells detected by flow cytometry analysis. Control: cells transfected with siNC ( A , D , E , F , G , left) or empty vector ( D , right). ANOVA test followed by Dunnett’s post hoc test was conducted. n = 3. ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Journal: Cellular & Molecular Biology Letters

Article Title: H 2 S induces apoptosis of tumors with high IDO1 expression via NR4A1-BCL-2 and SOCS3 pathways

doi: 10.1186/s11658-026-00945-5

Figure Lengend Snippet: Effects of H 2 S on NR4A1-mediated intrinsic apoptosis of tumor cells with different expression level of IDO1. Cells were treated with NaHS (2 mM) or GYY4137 (400 μM) for 24 h. A , B Mitochondria in IDO1 knockdown MCF-7 cells detected by fluorescence staining. Magnification: 400×; scale bars represent 50 μm. C CF488-labeled Cyt C (green) in MCF-7 cells upon different treatments recorded by fluorescence microscopy. DAPI (blue) was used for nuclear staining. Representative image of three independent experiments is shown. Scale bars represent 10 μm. D Protein expressions of IDO1, BCL-2, and BAX in IDO1 knockdown MCF-7 cells and IDO1-overexpressing A549 cells detected by WB. Statistical plots are shown in Supplementary Fig. S2. E – G Apoptosis of NR4A1 knockdown MCF-7, SGC-7901, or A549 cells detected by flow cytometry analysis. Control: cells transfected with siNC ( A , D , E , F , G , left) or empty vector ( D , right). ANOVA test followed by Dunnett’s post hoc test was conducted. n = 3. ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Article Snippet: Antibodies used are listed as follows: GADPH (Bosterbio, cat. no. a00227-1, RRID:AB_2813842), IDO1 (Proteintech, cat. no. 66528-1-Ig, RRID:AB_2881891), BAX (Proteintech, cat. no. 50599-2-Ig, RRID:AB_2061561), BCL-2 (ABclonal, cat. no. A20777, RRID:AB_3678973), SOCS3 (Proteintech, cat. no. 66797-1-lg, RRID:AB_2882141), NR4A1 (ABclonal, cat. no. A24016, RRID: AB_3678975), pIDO1 targeting phosphorylated ITIM2 (Huabio, custom-made), HRP-conjugated anti-mouse secondary antibody (Epizyme, cat. no. LF101, RRID:AB_3083706), and anti-rabbit secondary antibody (Epizyme, cat. no. LF102, RRID:AB_3083707).

Techniques: Expressing, Knockdown, Fluorescence, Staining, Labeling, Microscopy, Flow Cytometry, Control, Transfection, Plasmid Preparation

$Effects of H 2 S on NR4A1 nuclear translocation in tumor cells with different expression level of IDO1. Cells were treated with NaHS (2 mM, A – F ), GYY4137 (400 μM, A – F ), or Kyn (150 μM, G – H ) for 24 h. A , B CF488-labeled NR4A1 (green) in MCF-7, SGC-7901, and A549 cells upon different treatments recorded by fluorescence microscopy. DAPI (blue) was used for nuclear staining. Magnification: 400×, scale bars represent 50 μm. C NR4A1 protein levels in cytosolic and nuclear fractions in MCF-7, SGC-7901, and A549 cells detected by WB. Total cellular NR4A1 (total) was used as internal control. Statistical plots are shown in Supplementary Fig. S3. D mRNA expression of Cartpt in MCF-7, SGC-7901, and A549 cells detected by qPCR. E Kyn levels in MCF-7, SGC-7901, and A549 cells detected by HPLC. F Binding of NR4A1 and BCL-2 in MCF-7 cells detected by co-iP. G NR4A1 protein levels in cytosolic and nuclear fractions in A549 cells detected by WB. Total cellular NR4A1 (total) was used as internal control. H mRNA expression of Cartpt in MCF-7 and SGC-7901 cells detected by qPCR. Student’s t -test and ANOVA test followed by Dunnett’s post hoc test were conducted. n = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001$

Journal: Cellular & Molecular Biology Letters

Article Title: H 2 S induces apoptosis of tumors with high IDO1 expression via NR4A1-BCL-2 and SOCS3 pathways

doi: 10.1186/s11658-026-00945-5

Figure Lengend Snippet: Effects of H 2 S on NR4A1 nuclear translocation in tumor cells with different expression level of IDO1. Cells were treated with NaHS (2 mM, A – F ), GYY4137 (400 μM, A – F ), or Kyn (150 μM, G – H ) for 24 h. A , B CF488-labeled NR4A1 (green) in MCF-7, SGC-7901, and A549 cells upon different treatments recorded by fluorescence microscopy. DAPI (blue) was used for nuclear staining. Magnification: 400×, scale bars represent 50 μm. C NR4A1 protein levels in cytosolic and nuclear fractions in MCF-7, SGC-7901, and A549 cells detected by WB. Total cellular NR4A1 (total) was used as internal control. Statistical plots are shown in Supplementary Fig. S3. D mRNA expression of Cartpt in MCF-7, SGC-7901, and A549 cells detected by qPCR. E Kyn levels in MCF-7, SGC-7901, and A549 cells detected by HPLC. F Binding of NR4A1 and BCL-2 in MCF-7 cells detected by co-iP. G NR4A1 protein levels in cytosolic and nuclear fractions in A549 cells detected by WB. Total cellular NR4A1 (total) was used as internal control. H mRNA expression of Cartpt in MCF-7 and SGC-7901 cells detected by qPCR. Student’s t -test and ANOVA test followed by Dunnett’s post hoc test were conducted. n = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Techniques: Translocation Assay, Expressing, Labeling, Fluorescence, Microscopy, Staining, Control, Binding Assay, Co-Immunoprecipitation Assay

$Effects of H 2 S on mice bearing wild-type (GL261) or IDO1-overexpressing GL261 (GL261 IDO1-OE) glioma. A Proliferations of GL261 IDO1-OE cells and GL261 cells upon treatment with NaHS (0–800 μM) or GYY4137 (0–800 μM) for 24 h detected by CCK-8 assay. n = 3. B Tumor weight. C Concentration of Trp, Kyn, and IDO1 activity (represented by Kyn/Trp*100) in mice serum detected by HPLC. D Apoptosis of tumors detected by TUNEL assay. CF488: green fluorescence signals for apoptotic cells. DAPI (blue) was used for nuclear staining. Magnification: 200×; scale bars represent 100 μm. E Protein levels of pIDO1, IDO1, BAX, and BCL-2 in tumor cells detected by WB. F NR4A1 protein levels in cytosolic and nuclear fractions in tumor cells detected by WB. Total cellular NR4A1 (total) was used as internal control. G Colocalization of IDO1 and SOCS3 in tumors detected by immunofluorescence analysis. Scale bars represent 50 μm. For panel D – G , representative images of six independent experiments are shown. ANOVA test followed by Dunnett’s post hoc test was conducted. n = 6. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001$

Journal: Cellular & Molecular Biology Letters

Article Title: H 2 S induces apoptosis of tumors with high IDO1 expression via NR4A1-BCL-2 and SOCS3 pathways

doi: 10.1186/s11658-026-00945-5

Figure Lengend Snippet: Effects of H 2 S on mice bearing wild-type (GL261) or IDO1-overexpressing GL261 (GL261 IDO1-OE) glioma. A Proliferations of GL261 IDO1-OE cells and GL261 cells upon treatment with NaHS (0–800 μM) or GYY4137 (0–800 μM) for 24 h detected by CCK-8 assay. n = 3. B Tumor weight. C Concentration of Trp, Kyn, and IDO1 activity (represented by Kyn/Trp*100) in mice serum detected by HPLC. D Apoptosis of tumors detected by TUNEL assay. CF488: green fluorescence signals for apoptotic cells. DAPI (blue) was used for nuclear staining. Magnification: 200×; scale bars represent 100 μm. E Protein levels of pIDO1, IDO1, BAX, and BCL-2 in tumor cells detected by WB. F NR4A1 protein levels in cytosolic and nuclear fractions in tumor cells detected by WB. Total cellular NR4A1 (total) was used as internal control. G Colocalization of IDO1 and SOCS3 in tumors detected by immunofluorescence analysis. Scale bars represent 50 μm. For panel D – G , representative images of six independent experiments are shown. ANOVA test followed by Dunnett’s post hoc test was conducted. n = 6. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Techniques: CCK-8 Assay, Concentration Assay, Activity Assay, TUNEL Assay, Fluorescence, Staining, Control, Immunofluorescence

A schematic overview of the effect of H 2 S on NR4A1-BCL-2 pathway and the codegradation of pIDO1 and SOCS3 in tumor cells with high or low IDO1 expression, which resulted in apoptosis of tumor cells with high IDO1 expression

Journal: Cellular & Molecular Biology Letters

Article Title: H 2 S induces apoptosis of tumors with high IDO1 expression via NR4A1-BCL-2 and SOCS3 pathways

doi: 10.1186/s11658-026-00945-5

Figure Lengend Snippet: A schematic overview of the effect of H 2 S on NR4A1-BCL-2 pathway and the codegradation of pIDO1 and SOCS3 in tumor cells with high or low IDO1 expression, which resulted in apoptosis of tumor cells with high IDO1 expression

Techniques: Expressing

Nur77 is enriched in early‐differentiated human CD8 + T cells. (A) Expression of Nur77 in CD8 + T cell subsets (according to the expression of CCR7 and CD45RA) upon stimulation with anti‐CD3/CD28 antibodies (1 µg/mL) for up to 48 h ( n = 3). (B) Left panels: Representative expression of Nur77 in TCF‐1 + and TCF‐1 − CCR7 + CD45RA + CD8 + T cells. Right panel: Frequencies of Nur77 + cells among TCF‐1 + and TCF‐1 − CD8 + T cell subsets. (C–E) Expression of CD127 (C), TCF‐1 (D), and T‐bet (E) in Nur77 + and Nur77 − populations among CD8 + T cell subsets upon polyclonal stimulation for 48 h. (F–J) Frequency of TNF‐α + (F), IL‐2 + (G), IFN‐γ + (H), TNF‐α + IL‐2 + IFN‐γ + (I), and CFSE lo (J) cells in Nur77 + and Nur77 − populations among CD8 + T cell subsets upon polyclonal stimulation for 48 h. (K) CD8 + T cells were stimulated with anti‐CD3/CD28 antibodies for 96 h. The median fluorescence intensity (MFI) of TCF‐1 among Nur77 + and Nur77 − CD8 + T cell subsets is shown. (L) Representative gating for the analysis of Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − cells in CD8+ T cell subsets. (M) Frequency of Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − subsets among CD8 + T cell subsets. (N) Frequency of IFN‐γ + TNF‐α + cells among Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − subsets. In (B–K) and (M–N), the p value of Wilcoxon test is shown. Data derived from at least two independent experiments. Symbols represent one individual, and lines indicate the median. TCF‐1 + , T cell factor 1 + ; NS, not statistically significant. * p < 0.05; ** p < 0.01.

Journal: European Journal of Immunology

Article Title: Nur77 Is Associated With Polyfunctional Properties in Virus‐Specific Human CD8 + T Cells

doi: 10.1002/eji.70202

Figure Lengend Snippet: Nur77 is enriched in early‐differentiated human CD8 + T cells. (A) Expression of Nur77 in CD8 + T cell subsets (according to the expression of CCR7 and CD45RA) upon stimulation with anti‐CD3/CD28 antibodies (1 µg/mL) for up to 48 h ( n = 3). (B) Left panels: Representative expression of Nur77 in TCF‐1 + and TCF‐1 − CCR7 + CD45RA + CD8 + T cells. Right panel: Frequencies of Nur77 + cells among TCF‐1 + and TCF‐1 − CD8 + T cell subsets. (C–E) Expression of CD127 (C), TCF‐1 (D), and T‐bet (E) in Nur77 + and Nur77 − populations among CD8 + T cell subsets upon polyclonal stimulation for 48 h. (F–J) Frequency of TNF‐α + (F), IL‐2 + (G), IFN‐γ + (H), TNF‐α + IL‐2 + IFN‐γ + (I), and CFSE lo (J) cells in Nur77 + and Nur77 − populations among CD8 + T cell subsets upon polyclonal stimulation for 48 h. (K) CD8 + T cells were stimulated with anti‐CD3/CD28 antibodies for 96 h. The median fluorescence intensity (MFI) of TCF‐1 among Nur77 + and Nur77 − CD8 + T cell subsets is shown. (L) Representative gating for the analysis of Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − cells in CD8+ T cell subsets. (M) Frequency of Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − subsets among CD8 + T cell subsets. (N) Frequency of IFN‐γ + TNF‐α + cells among Nur77 + TCF‐1 + , Nur77 − TCF‐1 + , and Nur77 − TCF‐1 − subsets. In (B–K) and (M–N), the p value of Wilcoxon test is shown. Data derived from at least two independent experiments. Symbols represent one individual, and lines indicate the median. TCF‐1 + , T cell factor 1 + ; NS, not statistically significant. * p < 0.05; ** p < 0.01.

Article Snippet: In addition, in independent experiments, cells were polyclonally or peptide‐stimulated and simultaneously treated with the Nur77 modulator Csn‐B at 1 μM (MedChemExpress) [ ].

Techniques: Expressing, Fluorescence, Derivative Assay

Nur77 is associated with polyfunctional SARS‐CoV‐2‐specific CD8 + T cell responses. Peripheral blood mononuclear cells from human donors with previous exposure to SARS‐CoV‐2 were stimulated for 6 days with a peptide megapool derived from the proteome of the SARS‐CoV‐2 Wuhan ancestral strain to assess the naturally induced CD8 + T cell response. (A) Representative gating strategy and expression of selected markers in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (B) Frequencies of Nur77 + and Nur77 − cells among SARS‐CoV‐2‐specific CD8 + T cells. (C) Expression of CCR7, CD127, TCF‐1, and T‐bet in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (D) Frequency of CFSE lo cells in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (E) Expression of TNF‐α, IL‐2, and IFN‐γ in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (F–G) Frequency of TNF‐α + IL‐2 + (F) and TNF‐α + IL‐2 + IFN‐γ + (G) cells in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. In (B–G), the p value of Wilcoxon test is shown. Data derived from four independent experiments. Symbols represent one individual, and lines indicate the median. NS, not statistically significant; SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: European Journal of Immunology

Article Title: Nur77 Is Associated With Polyfunctional Properties in Virus‐Specific Human CD8 + T Cells

doi: 10.1002/eji.70202

Figure Lengend Snippet: Nur77 is associated with polyfunctional SARS‐CoV‐2‐specific CD8 + T cell responses. Peripheral blood mononuclear cells from human donors with previous exposure to SARS‐CoV‐2 were stimulated for 6 days with a peptide megapool derived from the proteome of the SARS‐CoV‐2 Wuhan ancestral strain to assess the naturally induced CD8 + T cell response. (A) Representative gating strategy and expression of selected markers in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (B) Frequencies of Nur77 + and Nur77 − cells among SARS‐CoV‐2‐specific CD8 + T cells. (C) Expression of CCR7, CD127, TCF‐1, and T‐bet in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (D) Frequency of CFSE lo cells in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (E) Expression of TNF‐α, IL‐2, and IFN‐γ in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. (F–G) Frequency of TNF‐α + IL‐2 + (F) and TNF‐α + IL‐2 + IFN‐γ + (G) cells in Nur77 + and Nur77 − SARS‐CoV‐2‐specific CD8 + T cells. In (B–G), the p value of Wilcoxon test is shown. Data derived from four independent experiments. Symbols represent one individual, and lines indicate the median. NS, not statistically significant; SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2. * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Derivative Assay, Expressing

Nur77 is associated with polyfunctional HIV‐specific CD8 + T cell responses. Peripheral blood mononuclear cells from people with HIV/HBV coinfection were stimulated for 6 days with a peptide megapool derived from the whole HIV proteome. (A) Representative gating strategy and expression of selected markers in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (B) Frequencies of Nur77 + and Nur77 − cells among HIV‐specific CD8 + T cells. (C) Expression of CCR7, CD127, TCF‐1, and T‐bet in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (D) Frequency of CFSE lo cells in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (E) Expression of TNF‐α, IL‐2, and IFN‐γ in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (F–G) Frequency of TNF‐α + IL‐2 + (F), and TNF‐α + IL‐2 + IFN‐γ + (G) cells in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. In (B–G), the p value of Wilcoxon test is shown. Data derived from four independent experiments. Symbols represent one individual, and lines indicate the median. HIV, human immunodeficiency virus; NS, not statistically significant. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: European Journal of Immunology

Article Title: Nur77 Is Associated With Polyfunctional Properties in Virus‐Specific Human CD8 + T Cells

doi: 10.1002/eji.70202

Figure Lengend Snippet: Nur77 is associated with polyfunctional HIV‐specific CD8 + T cell responses. Peripheral blood mononuclear cells from people with HIV/HBV coinfection were stimulated for 6 days with a peptide megapool derived from the whole HIV proteome. (A) Representative gating strategy and expression of selected markers in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (B) Frequencies of Nur77 + and Nur77 − cells among HIV‐specific CD8 + T cells. (C) Expression of CCR7, CD127, TCF‐1, and T‐bet in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (D) Frequency of CFSE lo cells in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (E) Expression of TNF‐α, IL‐2, and IFN‐γ in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. (F–G) Frequency of TNF‐α + IL‐2 + (F), and TNF‐α + IL‐2 + IFN‐γ + (G) cells in Nur77 + and Nur77 − HIV‐specific CD8 + T cells. In (B–G), the p value of Wilcoxon test is shown. Data derived from four independent experiments. Symbols represent one individual, and lines indicate the median. HIV, human immunodeficiency virus; NS, not statistically significant. * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Derivative Assay, Expressing, Virus

Nur77 modulation promotes Nur77 + TCF‐1 + polyfunctional human CD8 + T cells. Purified CD8 + T cells from healthy donors were treated with vehicle control or reprogrammed with a GSK3 inhibitor, followed by stimulation with anti‐CD3/CD28 antibodies and hrICAM‐1, for 48 h. (A) Left: representative expression of Nur77 in reprogrammed and non‐reprogrammed CD8 + T cells, upon polyclonal stimulation. Right: fold change in the frequency of Nur77 + cells in reprogrammed CD8 + T cells, relative to non‐reprogrammed cells. (B) Fold change in Nur77 expression in TCF‐1 + or TCF‐1 − reprogrammed CD8 + T cells, relative to non‐reprogrammed cells. In (A) and (B), the median and interquartile ranges are shown ( n = 8). (C–F) Purified CD8 + T cells from healthy donors were polyclonally stimulated with anti‐CD3/CD28 antibodies in the presence or absence of cytosporone B (Csn‐B), for 48 h. (C) Left: representative expression of Nur77 upon stimulation in Csn‐B‐treated and untreated cells. Right: frequency of Nur77 + CD8 + T cells upon the indicated treatments. (D) Expression of TCF‐1 upon polyclonal stimulation in Csn‐B‐treated and untreated CD8 + T cell subsets. (E–F) Frequencies of Nur77 + TCF‐1 + cells (E), and IFN‐γ + TNF‐α + cells among Nur77 + TCF‐1 + CD8 + T cell subsets (F), in Csn‐B‐treated and untreated cells. In (B–F), the p value of Wilcoxon test is shown. Data derived from at least two independent experiments. Symbols represent one individual, and lines indicate the median. TCF‐1 + , T cell factor 1 + ; NS, not statistically significant. * p < 0.05.

Journal: European Journal of Immunology

Article Title: Nur77 Is Associated With Polyfunctional Properties in Virus‐Specific Human CD8 + T Cells

doi: 10.1002/eji.70202

Figure Lengend Snippet: Nur77 modulation promotes Nur77 + TCF‐1 + polyfunctional human CD8 + T cells. Purified CD8 + T cells from healthy donors were treated with vehicle control or reprogrammed with a GSK3 inhibitor, followed by stimulation with anti‐CD3/CD28 antibodies and hrICAM‐1, for 48 h. (A) Left: representative expression of Nur77 in reprogrammed and non‐reprogrammed CD8 + T cells, upon polyclonal stimulation. Right: fold change in the frequency of Nur77 + cells in reprogrammed CD8 + T cells, relative to non‐reprogrammed cells. (B) Fold change in Nur77 expression in TCF‐1 + or TCF‐1 − reprogrammed CD8 + T cells, relative to non‐reprogrammed cells. In (A) and (B), the median and interquartile ranges are shown ( n = 8). (C–F) Purified CD8 + T cells from healthy donors were polyclonally stimulated with anti‐CD3/CD28 antibodies in the presence or absence of cytosporone B (Csn‐B), for 48 h. (C) Left: representative expression of Nur77 upon stimulation in Csn‐B‐treated and untreated cells. Right: frequency of Nur77 + CD8 + T cells upon the indicated treatments. (D) Expression of TCF‐1 upon polyclonal stimulation in Csn‐B‐treated and untreated CD8 + T cell subsets. (E–F) Frequencies of Nur77 + TCF‐1 + cells (E), and IFN‐γ + TNF‐α + cells among Nur77 + TCF‐1 + CD8 + T cell subsets (F), in Csn‐B‐treated and untreated cells. In (B–F), the p value of Wilcoxon test is shown. Data derived from at least two independent experiments. Symbols represent one individual, and lines indicate the median. TCF‐1 + , T cell factor 1 + ; NS, not statistically significant. * p < 0.05.

Techniques: Purification, Control, Expressing, Derivative Assay

Nur77 modulation enhances the functionality of HIV‐specific CD8 + T cells. Peripheral blood mononuclear cells from people with HIV/HBV coinfection were stimulated for 6 days with an HIV peptide megapool in the presence or absence of Csn‐B. (A) Left: representative expression of IFN‐γ and TNF‐α for the analysis of HIV‐specific CD8 + T cells. Right: frequency of HIV‐specific CD8 + T cells in Csn‐B‐treated and untreated cells. (B) Frequency of Nur77 + cells among HIV‐specific CD8 + T cells. (C) Expression of TCF‐1 in HIV‐specific CD8 + T cells. (D and E) Frequency of CFSE lo (D) and IFN‐γ + TNF‐α + (E) HIV‐specific CD8 + T cells. Data derived from two independent experiments. Symbols represent one individual, and lines indicate the median. p value of Wilcoxon test. Csn‐B, cytosporone B; HIV, human immunodeficiency virus. * p < 0.05; ** p < 0.001.

Journal: European Journal of Immunology

Article Title: Nur77 Is Associated With Polyfunctional Properties in Virus‐Specific Human CD8 + T Cells

doi: 10.1002/eji.70202

Figure Lengend Snippet: Nur77 modulation enhances the functionality of HIV‐specific CD8 + T cells. Peripheral blood mononuclear cells from people with HIV/HBV coinfection were stimulated for 6 days with an HIV peptide megapool in the presence or absence of Csn‐B. (A) Left: representative expression of IFN‐γ and TNF‐α for the analysis of HIV‐specific CD8 + T cells. Right: frequency of HIV‐specific CD8 + T cells in Csn‐B‐treated and untreated cells. (B) Frequency of Nur77 + cells among HIV‐specific CD8 + T cells. (C) Expression of TCF‐1 in HIV‐specific CD8 + T cells. (D and E) Frequency of CFSE lo (D) and IFN‐γ + TNF‐α + (E) HIV‐specific CD8 + T cells. Data derived from two independent experiments. Symbols represent one individual, and lines indicate the median. p value of Wilcoxon test. Csn‐B, cytosporone B; HIV, human immunodeficiency virus. * p < 0.05; ** p < 0.001.

Techniques: Expressing, Derivative Assay, Virus

Study design. 12–14 week old male Nur77 GFP mice underwent tMCAO, transient middle cerebral artery occlusion. At the timepoint of reperfusion, mice were injected intraperitoneally with LPS (40 µg/kg) or vehicle (PBS). Two hours after tMCAO and daily in the morning, mice were injected intraperitoneally with Soraphen A (SorA, 2.5 µmol/kg) or vehicle (PEG buffer). Magnetic resonance imaging (MRI) was conducted 16 hours and 7 days after tMCAO to verify infarct induction and calculate lesion volumes. Mice were scored daily and a set of behavioral tests (corner tests, cylinder test and inclined plane test) was conducted before as well as 2 and 6 days after tMCAO. At each experimental time point (16 h, 2 d, 3 d, 7 d after MCAO) brain, lungs, spleen, blood and ingiunal lymph nodes (ILN) were harvested and prepared for flow cytometric analysis of T cell activation and polarization, differentiating between antigen-specific and -unspecific T cell activation via GFP expression. To evaluate the impact of SorA treatment on stroke pathology under post-stroke and post-stroke inflammatory conditions associated with infection, we compared treatment groups to assess: the effect of LPS alone (vehicle/vehicle vs. LPS/vehicle), the effect of SorA alone (vehicle/vehicle vs. vehicle/SorA), and the effect of SorA under proinflammatory conditions (LPS/vehicle vs. LPS/SorA) in MCAO mice. Image created in BioRender. Vogelgesang, A. (2026) https://BioRender.com/pr62lu3 .

Journal: Frontiers in Immunology

Article Title: Targeting T cell metabolism and polarization to modulate post-stroke immune responses and improve outcomes

doi: 10.3389/fimmu.2026.1703552

Figure Lengend Snippet: Study design. 12–14 week old male Nur77 GFP mice underwent tMCAO, transient middle cerebral artery occlusion. At the timepoint of reperfusion, mice were injected intraperitoneally with LPS (40 µg/kg) or vehicle (PBS). Two hours after tMCAO and daily in the morning, mice were injected intraperitoneally with Soraphen A (SorA, 2.5 µmol/kg) or vehicle (PEG buffer). Magnetic resonance imaging (MRI) was conducted 16 hours and 7 days after tMCAO to verify infarct induction and calculate lesion volumes. Mice were scored daily and a set of behavioral tests (corner tests, cylinder test and inclined plane test) was conducted before as well as 2 and 6 days after tMCAO. At each experimental time point (16 h, 2 d, 3 d, 7 d after MCAO) brain, lungs, spleen, blood and ingiunal lymph nodes (ILN) were harvested and prepared for flow cytometric analysis of T cell activation and polarization, differentiating between antigen-specific and -unspecific T cell activation via GFP expression. To evaluate the impact of SorA treatment on stroke pathology under post-stroke and post-stroke inflammatory conditions associated with infection, we compared treatment groups to assess: the effect of LPS alone (vehicle/vehicle vs. LPS/vehicle), the effect of SorA alone (vehicle/vehicle vs. vehicle/SorA), and the effect of SorA under proinflammatory conditions (LPS/vehicle vs. LPS/SorA) in MCAO mice. Image created in BioRender. Vogelgesang, A. (2026) https://BioRender.com/pr62lu3 .

Article Snippet: The Nur77 GFP mouse model was generated by Kristin Hogquist (C57BL/6-Tg(Nr4a1-EGFP/cre)820Khog/J mice, Stock No: 016617, The Jackson Laboratory) ( ) and express eGFP under the control of the Nr4a1 promoter/enhancer regions.

Techniques: Injection, Magnetic Resonance Imaging, Activation Assay, Expressing, Infection

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