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