Intestinal Epithelial Cells Upregulate MHC Class II and Antigen Presentation Pathways During Experimental Autoimmune Encephalomyelitis
The intestinal epithelium plays a critical role in immune microbiota interactions; however, its contribution to systemic autoimmunity remains incompletely understood. Here, we profiled transcriptional changes in intestinal epithelial cells during experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Specific-pathogen-free (SPF) C57BL/6J mice were immunized with myelin oligodendrocyte glycoprotein peptide (MOG35_55) to induce EAE and were euthanized on day 24 post-immunization; non-immunized littermates served as controls. Ileal epithelial layers were enriched by EDTA/DTT based epithelial dissociation, followed by collection of epithelial fractions. Total RNA was extracted using TRIzol, and RNA quality and quantity were assessed prior to library preparation. RNAseq libraries were prepared from total RNA and sequenced on an Illumina platform to generate paired end reads. Sequencing reads were quality controlled, trimmed as needed, and aligned to the mouse reference genome; gene level counts were generated for downstream differential expression and pathway enrichment analyses. These data provide a resource for investigating epithelial immune-related transcriptional programs, including MHC class II and antigen presentation pathways, during EAE.