anti murine ifnar1 mab  (Bio X Cell)

Journal: bioRxiv

Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

doi: 10.64898/2026.03.02.709022

Figure Lengend Snippet: (A) Feature plots of IFN receptors, including IFN-I receptor ( IFNAR1/IFNAR2 ), IFN-II receptor ( IFNGR1/IFNGR2 ), IFN-III receptor ( IFNLR1/IL10RB ), in epithelial cells and CD14 + myeloid cells, from the scRNA-seq analysis of human colonic biopsies in . (B) Feature plots of IFN receptors, from the scRNA-seq analysis of DSS-induced colitis in . (C) Flow cytometry analysis of IFNAR1 + cells in mouse colon with or without DSS exposure, gated by immune cell marker CD45 and epithelial cell marker EpCAM. (D) Proportions of IFNAR1 + cells classified as immune cells (CD45 + /EpCAM - ) or epithelial cells (CD45 - /EpCAM + ) in mouse colon with or without DSS exposure. n=5 per group. (E-F) Flow cytometry analysis and quantification of median fluorescence intensity (MFI) of IFNAR1 expression in immune cells (CD45 + /EpCAM - ) and epithelial cells (CD45 - /EpCAM + ) from DSS-treated mouse colon.

Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

Techniques: Flow Cytometry, Marker, Fluorescence, Expressing

Journal: bioRxiv

Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

doi: 10.64898/2026.03.02.709022

Figure Lengend Snippet: (A) Schematic illustrating how the serine-to-alanine substitution at position 535 of murine IFNAR1 protein affects phosphorylation and ubiquitination-dependent degradation. (B) qRT-PCR analysis of selected IFN-I signature genes in spleen and colon from WT and SA mice at baseline. Data were normalized to the mean of WT mice (set as 1). n=5-10 per group. (C) qRT-PCR analysis of selected IFN-I signature genes in bone marrow-derived macrophages (BMDMs) from WT and SA mice, at baseline (untreated) and after stimulation by interferon-β (IFNβ, 200 IU/mL x 8 hours) or lipopolysaccharides (LPS, 1 µg/mL x 8 hours). Data were normalized to the mean of WT BMDMs at baseline (set as 1). n=5-10 per group. (D-E) Mass cytometry (CyTOF) analysis of colon from WT (n=4) and SA (n=6) mice at baseline. (D) UMAP plots with cells colored by identity. (E) Proportions of immune cells (CD45 + /EpCAM - ), epithelial cells (CD45 - /EpCAM + ), and stromal cells (CD45 - /EpCAM - ). ns: not significant. (F) Heatmap showing the mean expression of target proteins in the antibody panel (Supplemental Table 4), with those having p <0.05 by SAM (Significance Analysis of Microarrays) for their median expression indicated by red asterisks.

Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

Techniques: Phospho-proteomics, Ubiquitin Proteomics, Quantitative RT-PCR, Derivative Assay, Mass Cytometry, Expressing

Journal: bioRxiv

Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

doi: 10.64898/2026.03.02.709022

Figure Lengend Snippet: Weight change (A and E) , clinical disease activity index (CDAI) (B and F) , colon length (C and G) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (D and H) in colon in DSS-induced colitis (A-D) and piroxicam-accelerated enterocolitis (E-H) . (I-P) Schematics of experimental design (I and M) , clinical disease activity index (CDAI) (J and N) , colon length (K and O) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (L and P) to assess the effect of tamoxifen-induced knockout of IFNAR1 (I-L) and administration of blocking anti-IFNAR1 antibody (M-P) on DSS-induced colitis.

Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

Techniques: Activity Assay, Quantitative RT-PCR, Knock-Out, Blocking Assay

Journal: Biochemistry and Biophysics Reports

Article Title: Innate immune overactivation hinders nuclear reprogramming through IFN-IFNAR1 axis

doi: 10.1016/j.bbrep.2025.102395

Figure Lengend Snippet: PIC increased Ifnar1 surface expression and activated Ifnar1-stat1 signaling. In the CT group, dox-inducible OSKM MEFs were treated with dox every other day to initiate nuclear reprogramming. In the PIC group, PIC at a concentration of 1000 ng/ml was administered every other day for the first 6 days in addition to dox treatment. A. Representative FACS histogram of Ifnar1 in MEFs collected at indicated time points. The red curve represents the PIC group. The dark shaded curve represents the CT group. The light shaded curve represents a negative staining control. B. Quantification of MFI of Ifnar1. C. Ifnar1 gene expression in MEFs treated with CT and PIC, collected at specified time points. D. Western blot analysis of Stat1 expression from nuclear and whole-cell lysates. All data are presented as mean ± S.E.M. ∗, P < 0.05 compared to the CT group.

Article Snippet: Anti-mouse Ifnar1 (clone MAR1-5A3) antibody, APC-Ifnar1 antibody and mouse IgG1 antibody was from Leinco Technologies.

Techniques: Expressing, Concentration Assay, Negative Staining, Control, Gene Expression, Western Blot

Journal: Biochemistry and Biophysics Reports

Article Title: Innate immune overactivation hinders nuclear reprogramming through IFN-IFNAR1 axis

doi: 10.1016/j.bbrep.2025.102395

Figure Lengend Snippet: Antibodies blocking the Ifn-Ifnar1 axis restore PIC-impaired nuclear reprogramming. In the CT group, dox-inducible OSKM MEFs were treated with dox every other day to initiate nuclear reprogramming. In the PIC group, cells were treated with 1000 ng/ml PIC every other day for the first 6 days, in addition to dox treatment. In certain experimental groups, cells received treatment with Ifn-β neutralizing antibody or its control hamster IgG antibody, as well as Ifnar1 blocking antibody or its control mouse IgG antibody, every other day for the initial 8 days. A. Schematic representation of the experimental design. B. Representative images of iPSC colonies stained with AP (Alkaline Phosphatase). C. Quantification of iPSC colonies. All data are presented as mean ± S.E.M. ∗, P < 0.05 compared to the CT group; #, P < 0.05 compared to the IgG control-treated group.

Article Snippet: Anti-mouse Ifnar1 (clone MAR1-5A3) antibody, APC-Ifnar1 antibody and mouse IgG1 antibody was from Leinco Technologies.

Techniques: Blocking Assay, Control, Staining

Journal: Biochemistry and Biophysics Reports

Article Title: Innate immune overactivation hinders nuclear reprogramming through IFN-IFNAR1 axis

doi: 10.1016/j.bbrep.2025.102395

Figure Lengend Snippet: PIC treatment did not change the proliferation and apoptosis of OSKM-MEFs. In the CT group, dox-inducible OSKM MEFs were exposed to dox every other day to initiate nuclear reprogramming. In the PIC group, PIC was administered at a concentration of 1000 ng/mL every other day for the initial 6 days, in addition to dox treatment. In certain experimental groups, an Ifnar1 blocking antibody or its control, a mouse IgG antibody, was administered every other day for the first 8 days. A. Ifng gene expression. B. Levels of Ifn-γ detected in the culture medium using ELISA. C. Quantification of the percentage of EdU + cells. D. Quantification of the percentage of Annexin V+ cells. All data are presented as mean ± S.E.M. ∗, P < 0.05 compared to the CT group.

Article Snippet: Anti-mouse Ifnar1 (clone MAR1-5A3) antibody, APC-Ifnar1 antibody and mouse IgG1 antibody was from Leinco Technologies.

Techniques: Concentration Assay, Blocking Assay, Control, Gene Expression, Enzyme-linked Immunosorbent Assay