Extended Data Fig. 3: lnc13−/−-DQ8 mice exhibit transcriptional and humoral features shared with human celiac disease.
From: The long noncoding RNA lnc13 restrains inflammatory responses to maintain oral tolerance to gluten
(a) Cross-species correlation of top DEGs between lnc13−/−-DQ8 mice and human CeD patients. Mouse DEGs were mapped to human homologs and compared to human biopsy data (GSE134900). Strong correlation observed for proinflammatory genes (Cxcl5, Saa2, Oas2). Correlation was calculated using Pearson’s correlation. (b) Per-gene fold change of differentially expressed immunoglobulin (Ig) transcripts in mouse LPL RNA-seq and human intestinal biopsies (GSE134900). Each dot represents one Ig gene. For the mouse dataset, values are calculated as the fold change of the group-mean expression in lnc13 KO-DQ8 relative to WT-DQ8 LPL RNA-seq. For the human dataset, values are calculated as the fold change of the group-mean expression in celiac disease (CeD) relative to healthy controls (HC). A horizontal line indicates no change (fold change = 1). (c) Serum antibody responses following gluten challenge. lnc13−/−-DQ8 mice exhibit elevated levels of: anti-gliadin IgG, anti-deamidated gliadin peptide (DGP) IgG, anti-tissue transglutaminase (tTG) IgG. Raw optical density (OD) values are shown. Results indicate systemic autoimmune reactivity to gluten-associated antigens (n=7 mice, across 5 independent experiments). Data are shown as mean ± s.e.m.; statistical significance calculated by two-tailed, unpaired student’s t-test. * p <0.05,** p<0.01, *** p<0.001, **** p<0.0001.
