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il13 hy p70568 recombinant proteins  (MedChemExpress)


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    Structured Review

    MedChemExpress il13 hy p70568 recombinant proteins
    Il13 Hy P70568 Recombinant Proteins, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+il+13/IL-13%2C+Human/10__1016_slash_j__gendis__2026__102386-37-9-22
    Average 95 stars, based on 8 article reviews
    il13 hy p70568 recombinant proteins - by Bioz Stars, 2026-11
    95/100 stars

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    Related Articles

    In Vitro:

    Article Title: Escin alleviates DNCB-induced atopic dermatitis-like symptoms by promoting autophagy activation and tight junction barrier restoration.
    Article Snippet: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by impaired skin barrier function and immune dysregulation.. Autophagy, a lysosome-dependent degradation pathway essential for removing unnecessary components, plays a crucial role in maintaining cellular homeostasis.. Defective autophagy has been implicated in AD pathogenesis, and enhancing autophagic activity represents a viable therapeutic strategy.

    Recombinant:

    Article Title: Escin alleviates DNCB-induced atopic dermatitis-like symptoms by promoting autophagy activation and tight junction barrier restoration.
    Article Snippet: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by impaired skin barrier function and immune dysregulation.. Autophagy, a lysosome-dependent degradation pathway essential for removing unnecessary components, plays a crucial role in maintaining cellular homeostasis.. Defective autophagy has been implicated in AD pathogenesis, and enhancing autophagic activity represents a viable therapeutic strategy.

    Article Title: hnRNPA2B1 Promotes Malignant Phenotype and Tumor Progression of Gastric Cancer Cells by Regulating Macrophage M2 Polarization.
    Article Snippet: To investigate the mechanism by which heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1) regulates the maturation of LncRNA MM2P to promote M2 polarization of macrophages in gastric cancer.. In vitro experiments showed that hnRNPA2B1 could promote M2 polarization of iBMDM cells, enhance the maturation and expression of MM2P, and increase STAT6 phosphorylation levels.. When MM2P was knocked out, hnRNPA2B1 could no longer further promote cell M2 polarization. iBMDM cells with hnRNPA2B1‐induced M2 polarization could enhance the metastasis and invasion of MFC cells, improve clonogenic ability, and increase cell viability.

    Article Title: DUSP14 attenuates airway inflammation and mucus hypersecretion in allergic asthma by regulating TAK1 activity.
    Article Snippet: Allergic asthma is characterized by persistent chronic airway inflammation, leading to mucus hypersecretion and airway hyperresponsiveness.. Dual-specificity phosphatase 14 (DUSP14), a member of the DUSP family, is a key regulator in various biological processes.. However, the function of DUSP14 in allergic asthma remains to be elucidated.

    Article Title: Upregulated Hexokinase-2 in Airway Epithelium Regulates Apoptosis and Drives Inflammation in Asthma via Peptidylprolyl Isomerase F.
    Article Snippet: .. HK2 (ProteinTech, Wuhan, China, 22029-1-AP, RRID: AB_11182717), PPIF (ProteinTech, Wuhan, China, 18466-1-AP, RRID: AB_2169273), VDAC1 (ProteinTech, Wuhan, China, 55259-1-AP, RRID: AB_10837225), Scgb1a1 (ProteinTech, Wuhan, China, 10490-1-AP,RRID: AB_2183285), β-actin (ProteinTech, Wuhan, China, 66009-1-Ig, RRID: AB_2687938), and IgG (ProteinTech, Wuhan, China, 98136-1-RR,RRID: AB_3672282), Poly (ADP-Ribose)Polymerase (PARP) (Cell Signaling Technology, Danvers, MA, USA, #9542,RRID: P09874), Bax (Cell Signaling Technology, Danvers, MA, USA, #2772,RRID: AB_2909613), cleaved caspase-3 (Cell Signaling Technology, Danvers, MA, USA, #9661,RRID: AB_2341188), caspase-3 (Cell Signaling Technology, Danvers, MA, USA, #9662,RRID: AB_344892), and B-cell lymphoma 2 protein (Bcl-2) (Abcam, Cambridge, MA, USA, ab182858,RRID: AB_182858), recombinant IL-4 (MedChemExpress, Monmouth Junction, NJ, USA, HYP70445), recombinant IL-13 (MedChemExpress, New Jersey, USA, HY-P70568), recombinant IL-6 (MedChemExpress, New Jersey, USA, HY-P7044), recombinant IL-8 (MedChemEx- press, HY-P70569), recombinant IL-1β (MedChemExpress, HY-P7028), recombinant IL-33 (MedChemExpress, HY-P7041), LPS (Sigma-Aldrich, St.Louis, MO, USA), HDM (Greer Laboratories, Lenoir, NC, USA, Lot#421176), recombinant TNF-α (PeproTech, London, UK, 300-01A-50UG), DMEM/F12 (BasalMedia, Shanghai, China, L310KJ), Pronase E (Solarbio, Beijing, China, P8360), retinoic acid (MedChemExpress, New Jersey, USA, HY-14649), epidermal growth factor (MedChemExpress, New Jersey, USA, HY-P7076), bovine pituitary extract (Macgene, Beijing, China, CC023), insulin (Macgene, Beijing, China, CC101), transferrin (Macgene, Beijing, China, CC-109), cholera toxin (Macgene, Beijing, China, CC104). ..

    other:

    Article Title: An SPP1-SOCS1 pathway constrains interferon responses in tumor-associated macrophages and shapes an immunosuppressive tumor microenvironment.
    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Protein Transport Inhibitor BD Bioscience Cat#555029 BD HorizonTM Brilliant Stain Buffer BD Bioscience Cat#566349 Recombinant Mouse Osteopontin/OPN Protein R&D Cat#441-OP-050 Recombinant Osteopontin/OPN, Mouse (HEK293, His) MCE Cat#HY-P78358 Recombinant IFN-alpha 14, Mouse MCE Cat#HY-P76401 Recombinant IFN-beta, Mouse MCE Cat#HY-P73130 Recombinant IFN-gamma, Mouse MCE Cat#HY-P70667 Azoxymethane (AOM) MP Biomedicals Cat#2180139.1 Dextran Sodium Sulfate (DSS) MP Biomedical Cat#216011080 SIS3 SELLECK Cat#S7959 Stattic MCE Cat#HY-13818 Galunisertib MCE Cat#HY-13226 Ciforadenant MCE Cat#HY-101978 Corn Oil MCE Cat#HY-Y1888 DMSO SIGMA Cat#D8418 Recombinant Murine IL-2 PEPROTECH Cat#212-12 Recombinant Murine IL-4 PEPROTECH Cat#214-14 Recombinant Murine IL-10 PEPROTECH Cat#210-10 Recombinant Murine IL-12 p70 PEPROTECH Cat#210-12 Recombinant IL-13, Mouse MCE Cat#HY-P70460 Recombinant TGF beta 1/TGFB1, Mouse MCE Cat#HY-P7117 Bafilomycin A1 MCE Cat#HY-100558 Bortezomib MCE Cat#HY-10227 Recombinant Murine MCSF PEPROTECH Cat#315-02 D-Luciferin, Potassium Salt Goldbio Cat#LUCK-2G Critical commercial assays Zombie NIRTM Fixable Viability Kit Biolegend Cat#423106 Tumor Dissociation Kit, mouse MILTENYI Cat#130-096-730 EasySepTM Mouse CD4+ T Cell Isolation Kit STEMCELL Cat#19852 EasySepTM Mouse CD8+ T Cell Isolation Kit STEMCELL Cat#19853 RNeasy Mini Kit QIAGEN Cat# 74104 FOXP3/Transcription Factor Staining Buffer Set Thermo Fisher Cat# 00-5532-00 RNA isolater Total RNA Extraction Reagent Vazyme Cat# R401-01-AA PrimeScript RT Reagent Kit Takara Cat# RR047A TB Green Premix Ex Taq kit Takara Cat# RR420A Anti-Flag Nanobody IP kit (Magarose) AlpaLifeBio Cat# KTSM1361 mMESSAGE mMACHINETM T7 Transcription Kit Thermo Fisher Cat#AM1344 LipofectamineTM MessengerMAXTM Transfection Reagent Thermo Fisher Cat#LMRNA001 HiPerFect Transfection Reagent QIAGEN Cat#301704 QIAquick Gel Extraction Kit QIAGEN Cat#28704 Anti-Flag Nanobody IP kit (Magarose) AlpaLifeBio Cat#KTSM1361 PANO 7-plex IHC kit Panovue Cat#10217100100 Deposited data Processed Bulk RNA-seq data This paper https://doi.org/10.6084/m9.figshare.



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    Tumor necrosis factor-like ligand 1A (TL1A) expression and secretion increase as asthma progresses. (A) Western blot analysis of TL1A protein expression in the lung tissues in the wild-type and ovalbumin (OVA)-induced model groups. (B) Changes in the cytokine concentrations of TL1A and immunoglobulin E (IgE) in serum over time following the final challenge in cases and controls. (C) Changes in the cytokine concentrations of TL1A, interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 13 <t>(IL-13),</t> and interferon gamma (IFN-γ) in bronchoalveolar lavage fluid (BAL) over time following the final challenge in cases and controls. (D) Schematic summarizing the timeline of the in vivo asthma modeling with different allergen exposure frequencies. (E) Comparison of total cell counts in the BAL in each group for different challenge numbers. (F) Comparison of IL-13 concentrations in BAL changed for different challenge numbers. (G) Representative plots showing changes in eosinophil counts for different challenge numbers. (H) Changes in IgE concentrations in blood samples for different challenge numbers. (I to K) Representative plots showing Masson staining, hematoxylin and eosin (HE) staining, and periodic acid–Schiff (PAS) staining of pulmonary airway tissue in mice for different challenge numbers. (L) Representative plots showing comparison of S100A4 + CD8 + effector memory T (Tem) cell counts for different challenge numbers. (M) Comparison of TL1A expression level in lung tissue samples from each group. (N and O) Comparison of TL1A concentrations in serum/BAL samples in each group. Data are presented as mean ± SD (error bars) from at least 3 independent experiments, with n = 6 mice per group per experiment (A and E to O). Time-course studies (B and C) used n = 6 mice per time point. * P < 0.05 and ** P < 0.01 compared with the respective control groups. Histological scoring and flow cytometry analysis were performed by investigators blinded to the experimental groups.
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    Tumor necrosis factor-like ligand 1A (TL1A) expression and secretion increase as asthma progresses. (A) Western blot analysis of TL1A protein expression in the lung tissues in the wild-type and ovalbumin (OVA)-induced model groups. (B) Changes in the cytokine concentrations of TL1A and immunoglobulin E (IgE) in serum over time following the final challenge in cases and controls. (C) Changes in the cytokine concentrations of TL1A, interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 13 <t>(IL-13),</t> and interferon gamma (IFN-γ) in bronchoalveolar lavage fluid (BAL) over time following the final challenge in cases and controls. (D) Schematic summarizing the timeline of the in vivo asthma modeling with different allergen exposure frequencies. (E) Comparison of total cell counts in the BAL in each group for different challenge numbers. (F) Comparison of IL-13 concentrations in BAL changed for different challenge numbers. (G) Representative plots showing changes in eosinophil counts for different challenge numbers. (H) Changes in IgE concentrations in blood samples for different challenge numbers. (I to K) Representative plots showing Masson staining, hematoxylin and eosin (HE) staining, and periodic acid–Schiff (PAS) staining of pulmonary airway tissue in mice for different challenge numbers. (L) Representative plots showing comparison of S100A4 + CD8 + effector memory T (Tem) cell counts for different challenge numbers. (M) Comparison of TL1A expression level in lung tissue samples from each group. (N and O) Comparison of TL1A concentrations in serum/BAL samples in each group. Data are presented as mean ± SD (error bars) from at least 3 independent experiments, with n = 6 mice per group per experiment (A and E to O). Time-course studies (B and C) used n = 6 mice per time point. * P < 0.05 and ** P < 0.01 compared with the respective control groups. Histological scoring and flow cytometry analysis were performed by investigators blinded to the experimental groups.
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    Tumor necrosis factor-like ligand 1A (TL1A) expression and secretion increase as asthma progresses. (A) Western blot analysis of TL1A protein expression in the lung tissues in the wild-type and ovalbumin (OVA)-induced model groups. (B) Changes in the cytokine concentrations of TL1A and immunoglobulin E (IgE) in serum over time following the final challenge in cases and controls. (C) Changes in the cytokine concentrations of TL1A, interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 13 <t>(IL-13),</t> and interferon gamma (IFN-γ) in bronchoalveolar lavage fluid (BAL) over time following the final challenge in cases and controls. (D) Schematic summarizing the timeline of the in vivo asthma modeling with different allergen exposure frequencies. (E) Comparison of total cell counts in the BAL in each group for different challenge numbers. (F) Comparison of IL-13 concentrations in BAL changed for different challenge numbers. (G) Representative plots showing changes in eosinophil counts for different challenge numbers. (H) Changes in IgE concentrations in blood samples for different challenge numbers. (I to K) Representative plots showing Masson staining, hematoxylin and eosin (HE) staining, and periodic acid–Schiff (PAS) staining of pulmonary airway tissue in mice for different challenge numbers. (L) Representative plots showing comparison of S100A4 + CD8 + effector memory T (Tem) cell counts for different challenge numbers. (M) Comparison of TL1A expression level in lung tissue samples from each group. (N and O) Comparison of TL1A concentrations in serum/BAL samples in each group. Data are presented as mean ± SD (error bars) from at least 3 independent experiments, with n = 6 mice per group per experiment (A and E to O). Time-course studies (B and C) used n = 6 mice per time point. * P < 0.05 and ** P < 0.01 compared with the respective control groups. Histological scoring and flow cytometry analysis were performed by investigators blinded to the experimental groups.
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    Tumor necrosis factor-like ligand 1A (TL1A) expression and secretion increase as asthma progresses. (A) Western blot analysis of TL1A protein expression in the lung tissues in the wild-type and ovalbumin (OVA)-induced model groups. (B) Changes in the cytokine concentrations of TL1A and immunoglobulin E (IgE) in serum over time following the final challenge in cases and controls. (C) Changes in the cytokine concentrations of TL1A, interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 13 (IL-13), and interferon gamma (IFN-γ) in bronchoalveolar lavage fluid (BAL) over time following the final challenge in cases and controls. (D) Schematic summarizing the timeline of the in vivo asthma modeling with different allergen exposure frequencies. (E) Comparison of total cell counts in the BAL in each group for different challenge numbers. (F) Comparison of IL-13 concentrations in BAL changed for different challenge numbers. (G) Representative plots showing changes in eosinophil counts for different challenge numbers. (H) Changes in IgE concentrations in blood samples for different challenge numbers. (I to K) Representative plots showing Masson staining, hematoxylin and eosin (HE) staining, and periodic acid–Schiff (PAS) staining of pulmonary airway tissue in mice for different challenge numbers. (L) Representative plots showing comparison of S100A4 + CD8 + effector memory T (Tem) cell counts for different challenge numbers. (M) Comparison of TL1A expression level in lung tissue samples from each group. (N and O) Comparison of TL1A concentrations in serum/BAL samples in each group. Data are presented as mean ± SD (error bars) from at least 3 independent experiments, with n = 6 mice per group per experiment (A and E to O). Time-course studies (B and C) used n = 6 mice per time point. * P < 0.05 and ** P < 0.01 compared with the respective control groups. Histological scoring and flow cytometry analysis were performed by investigators blinded to the experimental groups.

    Journal: Research

    Article Title: Integrated Single-Cell Profiling Reveals TL1A as a Biomarker and Driver of Type 2 Inflammation via Macrophage-Dependent Immunoregulation in Asthma

    doi: 10.34133/research.1190

    Figure Lengend Snippet: Tumor necrosis factor-like ligand 1A (TL1A) expression and secretion increase as asthma progresses. (A) Western blot analysis of TL1A protein expression in the lung tissues in the wild-type and ovalbumin (OVA)-induced model groups. (B) Changes in the cytokine concentrations of TL1A and immunoglobulin E (IgE) in serum over time following the final challenge in cases and controls. (C) Changes in the cytokine concentrations of TL1A, interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 13 (IL-13), and interferon gamma (IFN-γ) in bronchoalveolar lavage fluid (BAL) over time following the final challenge in cases and controls. (D) Schematic summarizing the timeline of the in vivo asthma modeling with different allergen exposure frequencies. (E) Comparison of total cell counts in the BAL in each group for different challenge numbers. (F) Comparison of IL-13 concentrations in BAL changed for different challenge numbers. (G) Representative plots showing changes in eosinophil counts for different challenge numbers. (H) Changes in IgE concentrations in blood samples for different challenge numbers. (I to K) Representative plots showing Masson staining, hematoxylin and eosin (HE) staining, and periodic acid–Schiff (PAS) staining of pulmonary airway tissue in mice for different challenge numbers. (L) Representative plots showing comparison of S100A4 + CD8 + effector memory T (Tem) cell counts for different challenge numbers. (M) Comparison of TL1A expression level in lung tissue samples from each group. (N and O) Comparison of TL1A concentrations in serum/BAL samples in each group. Data are presented as mean ± SD (error bars) from at least 3 independent experiments, with n = 6 mice per group per experiment (A and E to O). Time-course studies (B and C) used n = 6 mice per time point. * P < 0.05 and ** P < 0.01 compared with the respective control groups. Histological scoring and flow cytometry analysis were performed by investigators blinded to the experimental groups.

    Article Snippet: The recombinant proteins, small-molecular compounds, or inhibitors were purchased as indicated: recombinant mouse IL-13, IL-33, and TSLP protein (MCE); recombinant human IL-2, IL-4, TNF-α, and IFN-γ protein (Abbkine); poly(I:C) (Selleck); lipopolysaccharide (Sigma-Aldrich); IL-1β (Thermo Fisher); and small-molecule inhibitors BAY11-7082, LY294002, PD98059, SB203580, and SP600125 (Selleck).

    Techniques: Expressing, Western Blot, In Vivo, Comparison, Staining, Control, Flow Cytometry

    Myeloid-cell-specific Tnfsf15 -knockout resulted in the attenuation of allergic airway inflammation. (A) Myeloid-cell-specific Tnfsf15 -knockout strategy. (B) Genotyping was confirmed using tail DNA genomic polymerase chain reaction. (C) Immunomagnetic bead sorting was used to isolate F4/80 + cells, and the expression level of tumor necrosis factor-like ligand 1A (TL1A) was quantified using Western blotting. (D to G) Representative plots showing the proportions of 4 major types of immune cells (macrophages, CD8 + T cells, CD4 + T cells, and B cells) infiltrating the lung tissues in each group. (H) Representative hematoxylin and eosin (HE) staining among the different groups and quantification of the airway inflammation score. Black scale bar, 50 µm. (I) Representative periodic acid–Schiff (PAS) staining among the different groups and quantification of the airway mucus score. (J) Representative Masson’s trichrome staining among the different groups and quantification of the collagen volume fraction. (K and L) Lung eosinophil or neutrophil counts, as determined by flow cytometry. (M) Total cell counts in bronchoalveolar lavage fluid (BAL). (N) Concentrations of interleukin 4 (IL-4) in BAL. (O) Concentrations of interleukin 13 (IL-13) in BAL. Data are presented as mean ± SD. Experiments were repeated 3 times with n = 6 to 8 mice per group per experiment. Cell sorting and Western blot (C) used pooled cells from n = 4 mice. Flow cytometry analyses (D to G and K) and histological scoring (H to J) were performed by investigators blinded to genotype and treatment. * P < 0.05 and ** P < 0.01 compared with the respective groups.

    Journal: Research

    Article Title: Integrated Single-Cell Profiling Reveals TL1A as a Biomarker and Driver of Type 2 Inflammation via Macrophage-Dependent Immunoregulation in Asthma

    doi: 10.34133/research.1190

    Figure Lengend Snippet: Myeloid-cell-specific Tnfsf15 -knockout resulted in the attenuation of allergic airway inflammation. (A) Myeloid-cell-specific Tnfsf15 -knockout strategy. (B) Genotyping was confirmed using tail DNA genomic polymerase chain reaction. (C) Immunomagnetic bead sorting was used to isolate F4/80 + cells, and the expression level of tumor necrosis factor-like ligand 1A (TL1A) was quantified using Western blotting. (D to G) Representative plots showing the proportions of 4 major types of immune cells (macrophages, CD8 + T cells, CD4 + T cells, and B cells) infiltrating the lung tissues in each group. (H) Representative hematoxylin and eosin (HE) staining among the different groups and quantification of the airway inflammation score. Black scale bar, 50 µm. (I) Representative periodic acid–Schiff (PAS) staining among the different groups and quantification of the airway mucus score. (J) Representative Masson’s trichrome staining among the different groups and quantification of the collagen volume fraction. (K and L) Lung eosinophil or neutrophil counts, as determined by flow cytometry. (M) Total cell counts in bronchoalveolar lavage fluid (BAL). (N) Concentrations of interleukin 4 (IL-4) in BAL. (O) Concentrations of interleukin 13 (IL-13) in BAL. Data are presented as mean ± SD. Experiments were repeated 3 times with n = 6 to 8 mice per group per experiment. Cell sorting and Western blot (C) used pooled cells from n = 4 mice. Flow cytometry analyses (D to G and K) and histological scoring (H to J) were performed by investigators blinded to genotype and treatment. * P < 0.05 and ** P < 0.01 compared with the respective groups.

    Article Snippet: The recombinant proteins, small-molecular compounds, or inhibitors were purchased as indicated: recombinant mouse IL-13, IL-33, and TSLP protein (MCE); recombinant human IL-2, IL-4, TNF-α, and IFN-γ protein (Abbkine); poly(I:C) (Selleck); lipopolysaccharide (Sigma-Aldrich); IL-1β (Thermo Fisher); and small-molecule inhibitors BAY11-7082, LY294002, PD98059, SB203580, and SP600125 (Selleck).

    Techniques: Knock-Out, Polymerase Chain Reaction, Expressing, Western Blot, Staining, Flow Cytometry, FACS

    Identification of C-C motif chemokine ligand 8 (CCL8) as the key link in the tumor necrosis factor-like ligand 1A (TL1A)-induced allergic inflammatory response. (A) Heatmap showing changes in proallergic chemokine expression levels after gene knockdown. (B) Relative gene expression of CCL8 in lung tissue, quantified using polymerase chain reaction (PCR). (C) Relative gene expression of CCL8 in sorted F4/80 + cell groups in lung tissue, quantified using PCR. (D) CCL8 concentration in bronchoalveolar lavage fluid (BAL) measured using enzyme-linked immunosorbent assay (ELISA). (E) Relative gene expression of CCL8 in lung tissue, quantified using PCR in Tnfsf15 -knockout (KO) mice. (F) CCL8 concentration in BAL measured using ELISA in Tnfsf15 -KO mice. (G) CCL8 expression in the lung tissue of Tnfsf15 transgenic and nontransgenic mice. (H) The correlation between TL1A and CCL8 expression in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) cohort (based on GSE76262 ). (I) Schematic of the murine ovalbumin-induced asthma models following recombinant TL1A or anti-C-C motif chemokine receptor 8 (anti-CCR8) intervention. (J) Hematoxylin and eosin (HE) staining of lung tissue after allergen challenge and recombinant TL1A (rTL1A) or anti-CCR8 interventions. Black scale bar, 50 µm. (K) Total cell numbers in BAL samples. (L to N) Concentrations of CCL8, interleukin 4 (IL-4), and interleukin 13 (IL-13) in BAL samples from the different groups. Data are presented as mean ± SD from at least 2 independent experiments, with n = 5 to 6 mice per group per experiment. PCR, ELISA, and histological assessments were conducted by researchers blinded to treatment groups. Public dataset correlation (H) used n = samples from the GSE76262 dataset. * P < 0.05 and ** P < 0.01 compared with the respective groups.

    Journal: Research

    Article Title: Integrated Single-Cell Profiling Reveals TL1A as a Biomarker and Driver of Type 2 Inflammation via Macrophage-Dependent Immunoregulation in Asthma

    doi: 10.34133/research.1190

    Figure Lengend Snippet: Identification of C-C motif chemokine ligand 8 (CCL8) as the key link in the tumor necrosis factor-like ligand 1A (TL1A)-induced allergic inflammatory response. (A) Heatmap showing changes in proallergic chemokine expression levels after gene knockdown. (B) Relative gene expression of CCL8 in lung tissue, quantified using polymerase chain reaction (PCR). (C) Relative gene expression of CCL8 in sorted F4/80 + cell groups in lung tissue, quantified using PCR. (D) CCL8 concentration in bronchoalveolar lavage fluid (BAL) measured using enzyme-linked immunosorbent assay (ELISA). (E) Relative gene expression of CCL8 in lung tissue, quantified using PCR in Tnfsf15 -knockout (KO) mice. (F) CCL8 concentration in BAL measured using ELISA in Tnfsf15 -KO mice. (G) CCL8 expression in the lung tissue of Tnfsf15 transgenic and nontransgenic mice. (H) The correlation between TL1A and CCL8 expression in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) cohort (based on GSE76262 ). (I) Schematic of the murine ovalbumin-induced asthma models following recombinant TL1A or anti-C-C motif chemokine receptor 8 (anti-CCR8) intervention. (J) Hematoxylin and eosin (HE) staining of lung tissue after allergen challenge and recombinant TL1A (rTL1A) or anti-CCR8 interventions. Black scale bar, 50 µm. (K) Total cell numbers in BAL samples. (L to N) Concentrations of CCL8, interleukin 4 (IL-4), and interleukin 13 (IL-13) in BAL samples from the different groups. Data are presented as mean ± SD from at least 2 independent experiments, with n = 5 to 6 mice per group per experiment. PCR, ELISA, and histological assessments were conducted by researchers blinded to treatment groups. Public dataset correlation (H) used n = samples from the GSE76262 dataset. * P < 0.05 and ** P < 0.01 compared with the respective groups.

    Article Snippet: The recombinant proteins, small-molecular compounds, or inhibitors were purchased as indicated: recombinant mouse IL-13, IL-33, and TSLP protein (MCE); recombinant human IL-2, IL-4, TNF-α, and IFN-γ protein (Abbkine); poly(I:C) (Selleck); lipopolysaccharide (Sigma-Aldrich); IL-1β (Thermo Fisher); and small-molecule inhibitors BAY11-7082, LY294002, PD98059, SB203580, and SP600125 (Selleck).

    Techniques: Expressing, Knockdown, Gene Expression, Polymerase Chain Reaction, Concentration Assay, Enzyme-linked Immunosorbent Assay, Knock-Out, Transgenic Assay, Recombinant, Staining