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il 1r1  (Bio X Cell)


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    Structured Review

    Bio X Cell il 1r1
    Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows <t>IL-1R1</t> (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.
    Il 1r1, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/invivomab+anti+mouse+il+1r1+antibody/InVivoMAb+anti-mouse+IL-1+R/pm40238872-237-10-14
    Average 93 stars, based on 24 article reviews
    il 1r1 - by Bioz Stars, 2026-10
    93/100 stars

    Images

    1) Product Images from "Earlier onset of chemotherapy-induced neuropathic pain in females by ICAM-1-mediated accumulation of perivascular macrophages."

    Article Title: Earlier onset of chemotherapy-induced neuropathic pain in females by ICAM-1-mediated accumulation of perivascular macrophages.

    Journal: Science advances

    doi: 10.1126/sciadv.adu2159

    Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows IL-1R1 (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.
    Figure Legend Snippet: Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows IL-1R1 (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.

    Techniques Used: Immunofluorescence, Double Immunofluorescence Staining, Injection, Expressing, Immunostaining

    Related Articles

    Isolation:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Flow Cytometry:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Expressing:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Blocking Assay:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Control:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    MANN-WHITNEY:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Virus:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Recombinant:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Staining:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    SYBR Green Assay:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Protease Inhibitor:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Protein Extraction:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Bicinchoninic Acid Protein Assay:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Chromatography:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Library Quantification:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    SNP Genotyping Assay:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Gene Expression:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Microarray:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Infection:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Software:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Transfection:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Transferring:

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.



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    Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows <t>IL-1R1</t> (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.
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    Image Search Results


    Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows IL-1R1 (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.

    Journal: Science advances

    Article Title: Earlier onset of chemotherapy-induced neuropathic pain in females by ICAM-1-mediated accumulation of perivascular macrophages.

    doi: 10.1126/sciadv.adu2159

    Figure Lengend Snippet: Fig. 6. ICAM-1 and IL-1α released by endothelial cells synergistically promote macrophage infiltration in female mice following BTZ. (A) Il1a, Ccl5, and Ccl1 mRNA levels in the dorsal horn of female mice. n = 5 to 8. (B) Immunofluorescence image of IL-1α (green) in vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (C) Double immunofluorescence staining of CCL1 (green) and vascular endothelial cells (red). Scale bars, 50 μm (low) or 20 μm (high). (D and E) Coimmunostaining image of F4/80 (green) and CD31 (red) in the spinal dorsal horn and the statistical graph. Scale bar, 200 μm. n = 5. (F) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. (G) Immunofluorescence image shows IL-1R1 (red) expression in macrophages (green). Scale bar, 10 μm. (H and I) Intrathecal IL-1R1 injection inhibited the up-regulation of F4/80 (green) and CD31 (red) in the near vascular of the spinal dorsal horn. Scale bar, 200 μm (H). The number of F4/80high cells in the dorsal horn of the spinal cord [(I), left]. The percentage of F4/80high area among CD31+ area [(I), right]. n = 4 to 5. (J and K) Immunostaining shows F4/80 (green) and CD31 (red) expression in the spinal dorsal horn. Scale bar, 200 μm (J). The number of F4/80high cells in the dorsal horn of the spinal cord [(K), left]. The percentage of F4/80high area among CD31+ area [(K), right]. n = 5. (L) Intrathecal injection of IL-1α siRNA attenuated the mechanical allodynia induced by BTZ. n = 5. Significance: *P < 0.05, #P < 0.05, **P < 0.01, and ##P < 0.01.

    Article Snippet: For neutralizing antibodies CCL1 (20 μg/kg; R&D Systems, MAB845) and IL- 1R1 (20 μg/kg; Bio X Cell, BE0256), mice were administered intrathecally 30 min before the injection of BTZ or the IL1R1 ligand, IL- 1α.

    Techniques: Immunofluorescence, Double Immunofluorescence Staining, Injection, Expressing, Immunostaining

    Mice bearing 9-day-old orthotopic PDAC tumors (confirmed by luminescence imaging) were treated every 3 days with the indicated antibodies (200 µg/mouse, intraperitoneal). (a) Bulk transcriptomic analysis of orthotopic PDAC tumors after 2 weeks of treatment initiation (*p < 0.05; unpaired t-test, n = 2 mice/group). (b) Kaplan-Meier survival curves (log-rank test, n = 5-6 mice/group). (c) Tumor growth kinetics in subcutaneous PDAC-bearing mice treated every 3 days with agonistic CD40 antibody, anti-IL-1R1 antibody, their combination, or left untreated (****p < 0.0001; two-way ANOVA, n = 5-8 mice/group). (d) Representative H&E-stained tumor sections showing necrosis after 2 weeks of treatment (n = 3-4 mice/group). (e) Quantification of necrotic areas (**p < 0.01; one-way ANOVA, n = 3-4 mice/group). (f) Flow cytometric analysis of PMN-MDSCs in peripheral blood after 2 weeks of treatment (*p < 0.05; unpaired Student’s t-test, n = 5 mice/group). (g) Volcano plot of differentially expressed genes (DEGs) in subcutaneous PDAC tumors treated with anti-IL-1R1 versus untreated controls (red: upregulated; green: downregulated; 546 up, 530 down; p ≤ 0.05, log2FC ≥ 0). (h–i) Gene Ontology (GO) enrichment analysis of DEGs from (g), showing significantly upregulated (h) and downregulated (i) biological processes. (j) Volcano plot of DEGs comparing combination therapy (CD40 + anti-IL-1R1) versus CD40 monotherapy (524 up, 534 down; p ≤ 0.05, log2FC ≥ 0). (k–l) GO enrichment analysis of DEGs from (j), highlighting upregulated (k) and downregulated (l) pathways. (m) Gene Set Enrichment Analysis (GSEA) plots demonstrating the enrichment of indicated gene sets in the combination therapy group compared to CD40 monotherapy.

    Journal: bioRxiv

    Article Title: IL-1R1 Blockade Enhances CD40 Agonist-Mediated Immune Responses but Fails to Increase Efficacy or Mitigate Hepatotoxicity in Pancreatic Cancer

    doi: 10.1101/2025.02.23.639774

    Figure Lengend Snippet: Mice bearing 9-day-old orthotopic PDAC tumors (confirmed by luminescence imaging) were treated every 3 days with the indicated antibodies (200 µg/mouse, intraperitoneal). (a) Bulk transcriptomic analysis of orthotopic PDAC tumors after 2 weeks of treatment initiation (*p < 0.05; unpaired t-test, n = 2 mice/group). (b) Kaplan-Meier survival curves (log-rank test, n = 5-6 mice/group). (c) Tumor growth kinetics in subcutaneous PDAC-bearing mice treated every 3 days with agonistic CD40 antibody, anti-IL-1R1 antibody, their combination, or left untreated (****p < 0.0001; two-way ANOVA, n = 5-8 mice/group). (d) Representative H&E-stained tumor sections showing necrosis after 2 weeks of treatment (n = 3-4 mice/group). (e) Quantification of necrotic areas (**p < 0.01; one-way ANOVA, n = 3-4 mice/group). (f) Flow cytometric analysis of PMN-MDSCs in peripheral blood after 2 weeks of treatment (*p < 0.05; unpaired Student’s t-test, n = 5 mice/group). (g) Volcano plot of differentially expressed genes (DEGs) in subcutaneous PDAC tumors treated with anti-IL-1R1 versus untreated controls (red: upregulated; green: downregulated; 546 up, 530 down; p ≤ 0.05, log2FC ≥ 0). (h–i) Gene Ontology (GO) enrichment analysis of DEGs from (g), showing significantly upregulated (h) and downregulated (i) biological processes. (j) Volcano plot of DEGs comparing combination therapy (CD40 + anti-IL-1R1) versus CD40 monotherapy (524 up, 534 down; p ≤ 0.05, log2FC ≥ 0). (k–l) GO enrichment analysis of DEGs from (j), highlighting upregulated (k) and downregulated (l) pathways. (m) Gene Set Enrichment Analysis (GSEA) plots demonstrating the enrichment of indicated gene sets in the combination therapy group compared to CD40 monotherapy.

    Article Snippet: Beginning 9 days after tumor implantation, subcutaneous and orthotopic PDAC-bearing mice were treated with anti-IL-1R1 (Clone JAMA-147, BioXCell) or isotype control antibodies (BioXCell) administered intraperitoneally.

    Techniques: Imaging, Staining

    Mice bearing 9-day-old subcutaneous PDAC tumors were treated as indicated. (a-b) Serum ALT (a) and AST (b) levels were measured 48 hours after treatment initiation using the COBAS INTEGRA 400 Plus analyzer. *p < 0.01, Wilcoxon non-parametric test; n = 6-9 mice/group. Data represent results combined from two independent experiments. (c) Representative H&E-stained liver histology images from mice collected one week after treatment initiation (n = 3 mice/group, two treatments administered). (d) Cumulative quantification of immune infiltration and histological changes (n = 3 mice/group). (e-f) Serum ALT and AST levels measured after 9 days (e) and 3 weeks (f) of treatment initiation. Combo: agonistic CD40 + anti-IL-1R1 antibody. (g-h) Transcriptomic profiling of the liver from PDAC-bearing mice one week after treatment initiation (two treatments total). KEGG pathway enrichment analysis comparing agonistic CD40 vs. no treatment (g) and combo vs. agonistic CD40 (h). The dot plot highlights pathways associated with liver function, toxicity, and immune infiltration. Dot size represents the number of genes involved (Count), while color intensity reflects statistical significance (−log10 p-value). Upregulated pathways are marked with upward triangles (▴), and downregulated pathways with downward triangles (▾). Pathways with p-value < 0.05 are considered significantly enriched.

    Journal: bioRxiv

    Article Title: IL-1R1 Blockade Enhances CD40 Agonist-Mediated Immune Responses but Fails to Increase Efficacy or Mitigate Hepatotoxicity in Pancreatic Cancer

    doi: 10.1101/2025.02.23.639774

    Figure Lengend Snippet: Mice bearing 9-day-old subcutaneous PDAC tumors were treated as indicated. (a-b) Serum ALT (a) and AST (b) levels were measured 48 hours after treatment initiation using the COBAS INTEGRA 400 Plus analyzer. *p < 0.01, Wilcoxon non-parametric test; n = 6-9 mice/group. Data represent results combined from two independent experiments. (c) Representative H&E-stained liver histology images from mice collected one week after treatment initiation (n = 3 mice/group, two treatments administered). (d) Cumulative quantification of immune infiltration and histological changes (n = 3 mice/group). (e-f) Serum ALT and AST levels measured after 9 days (e) and 3 weeks (f) of treatment initiation. Combo: agonistic CD40 + anti-IL-1R1 antibody. (g-h) Transcriptomic profiling of the liver from PDAC-bearing mice one week after treatment initiation (two treatments total). KEGG pathway enrichment analysis comparing agonistic CD40 vs. no treatment (g) and combo vs. agonistic CD40 (h). The dot plot highlights pathways associated with liver function, toxicity, and immune infiltration. Dot size represents the number of genes involved (Count), while color intensity reflects statistical significance (−log10 p-value). Upregulated pathways are marked with upward triangles (▴), and downregulated pathways with downward triangles (▾). Pathways with p-value < 0.05 are considered significantly enriched.

    Article Snippet: Beginning 9 days after tumor implantation, subcutaneous and orthotopic PDAC-bearing mice were treated with anti-IL-1R1 (Clone JAMA-147, BioXCell) or isotype control antibodies (BioXCell) administered intraperitoneally.

    Techniques: Staining

    Mice bearing 9-day-old subcutaneous PDAC tumors were treated as indicated. Graphs show tumor growth at indicated time points. Figure: Tumor growth kinetics in mice bearing 9-day-old subcutaneous PDAC tumors treated as indicated. Tumor area (mm 2 ) was measured over 27 days following treatment initiation. Treatment groups included: no treatment (NO Tx), anti-Ly6G, agonistic CD40 (AgoCD40), AgoCD40 combined with anti-Ly6G, and AgoCD40 combined with anti-IL-1R1. Data represent mean ± SEM (n = 6-9 mice per group). Statistical significance was determined by two-way ANOVA with Tukey’s post hoc test. ***p < 0.001, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: IL-1R1 Blockade Enhances CD40 Agonist-Mediated Immune Responses but Fails to Increase Efficacy or Mitigate Hepatotoxicity in Pancreatic Cancer

    doi: 10.1101/2025.02.23.639774

    Figure Lengend Snippet: Mice bearing 9-day-old subcutaneous PDAC tumors were treated as indicated. Graphs show tumor growth at indicated time points. Figure: Tumor growth kinetics in mice bearing 9-day-old subcutaneous PDAC tumors treated as indicated. Tumor area (mm 2 ) was measured over 27 days following treatment initiation. Treatment groups included: no treatment (NO Tx), anti-Ly6G, agonistic CD40 (AgoCD40), AgoCD40 combined with anti-Ly6G, and AgoCD40 combined with anti-IL-1R1. Data represent mean ± SEM (n = 6-9 mice per group). Statistical significance was determined by two-way ANOVA with Tukey’s post hoc test. ***p < 0.001, ****p < 0.0001.

    Article Snippet: Beginning 9 days after tumor implantation, subcutaneous and orthotopic PDAC-bearing mice were treated with anti-IL-1R1 (Clone JAMA-147, BioXCell) or isotype control antibodies (BioXCell) administered intraperitoneally.

    Techniques:

    MNP FcγR A:I Ratio Modulates Intestinal Type 17 Immunity (A) Type-17-associated cytokine production by day-14 LPMCs stimulated with Ova and Ova-IC for 16 h (n = 5–9). Paired samples represent cells isolated from the same mouse. Data are pooled from 2 independent experiments. (B) qPCR of type 17 cytokines in WT and Fcgr2b −/− whole colonic tissue after cDSS versus controls (n = 4–9 per group). Data are normalized to uninflamed healthy colon. Medians are indicated. Data are representative of 2 independent experiments. (C) Flow-cytometry plots of colonic IL-17A-expressing T cell subsets in co-housed sex-matched WT and Fcgr2b −/− mice at day 21 after aDSS (n = 6–8 per group) versus controls (day 0) (n = 3–5 per group). (D) Quantification of absolute numbers of colonic IL-17A-producing T cells shown in (C). Medians are indicated. Data are representative of 3 independent experiments. (E) Quantification of absolute numbers of colonic IL-17A-producing T cell subsets in co-housed WT and Fcgr2b −/− mice at day 15 after aDSS and weekly treatment with anti-IL-1R1 IgG-blocking antibody or control IgG (n = 5–7 per group). Medians are indicated. Data are representative of two independent experiments. (F) Colonic IL-17A-expressing T cell subsets in M-TG and N-TG littermate controls at day 21 after aDSS (n = 5 or 6 per group) versus controls (n = 5 or 6 per group). Data are representative of two independent experiments. (G) Quantification of absolute cell counts of colonic IL-17A-producing T cell subsets as shown in (F). Medians are indicated. (H) Weight loss of Fcgr2b −/− mice treated with control or anti-IL-1R1 IgG antibodies after aDSS treatment (n = 5–7 per group). Mean ± SEM are indicated. Data are representative of two independent experiments. (I) Colonic neutrophil infiltration in WT and Fcgr2b −/− mice treated as in (H) (n = 5–7 per group). Medians are indicated. p values were calculated with a ratio paired t test (A), the nonparametric Mann-Whitney U test (B–G and I), or a two-way ANOVA (H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. See also <xref ref-type=Figure S6 . " width="100%" height="100%">

    Journal: Immunity

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis

    doi: 10.1016/j.immuni.2019.02.006

    Figure Lengend Snippet: MNP FcγR A:I Ratio Modulates Intestinal Type 17 Immunity (A) Type-17-associated cytokine production by day-14 LPMCs stimulated with Ova and Ova-IC for 16 h (n = 5–9). Paired samples represent cells isolated from the same mouse. Data are pooled from 2 independent experiments. (B) qPCR of type 17 cytokines in WT and Fcgr2b −/− whole colonic tissue after cDSS versus controls (n = 4–9 per group). Data are normalized to uninflamed healthy colon. Medians are indicated. Data are representative of 2 independent experiments. (C) Flow-cytometry plots of colonic IL-17A-expressing T cell subsets in co-housed sex-matched WT and Fcgr2b −/− mice at day 21 after aDSS (n = 6–8 per group) versus controls (day 0) (n = 3–5 per group). (D) Quantification of absolute numbers of colonic IL-17A-producing T cells shown in (C). Medians are indicated. Data are representative of 3 independent experiments. (E) Quantification of absolute numbers of colonic IL-17A-producing T cell subsets in co-housed WT and Fcgr2b −/− mice at day 15 after aDSS and weekly treatment with anti-IL-1R1 IgG-blocking antibody or control IgG (n = 5–7 per group). Medians are indicated. Data are representative of two independent experiments. (F) Colonic IL-17A-expressing T cell subsets in M-TG and N-TG littermate controls at day 21 after aDSS (n = 5 or 6 per group) versus controls (n = 5 or 6 per group). Data are representative of two independent experiments. (G) Quantification of absolute cell counts of colonic IL-17A-producing T cell subsets as shown in (F). Medians are indicated. (H) Weight loss of Fcgr2b −/− mice treated with control or anti-IL-1R1 IgG antibodies after aDSS treatment (n = 5–7 per group). Mean ± SEM are indicated. Data are representative of two independent experiments. (I) Colonic neutrophil infiltration in WT and Fcgr2b −/− mice treated as in (H) (n = 5–7 per group). Medians are indicated. p values were calculated with a ratio paired t test (A), the nonparametric Mann-Whitney U test (B–G and I), or a two-way ANOVA (H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. See also Figure S6 .

    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Techniques: Isolation, Flow Cytometry, Expressing, Blocking Assay, Control, MANN-WHITNEY

    Journal: Immunity

    Article Title: Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis

    doi: 10.1016/j.immuni.2019.02.006

    Figure Lengend Snippet:

    Article Snippet: InVivoMab anti-mouse IL-1R1 antibody , BioXCell , Cat#BE0256; RRID: AB_2661843.

    Techniques: Virus, Control, Recombinant, Staining, SYBR Green Assay, Protease Inhibitor, Protein Extraction, Enzyme-linked Immunosorbent Assay, Bicinchoninic Acid Protein Assay, Chromatography, Library Quantification, SNP Genotyping Assay, Gene Expression, Microarray, Infection, Software, Transfection, Transferring