Researchers at Keio University mapped a mechanistic gut–immune link to multiple sclerosis–related neuroinflammation, reporting that intestinal epithelial cells can drive encephalitogenic T-cell development through MHC class II. In mouse models of experimental autoimmune encephalomyelitis (EAE), deleting MHC II in intestinal epithelial cells reduced TH17 accumulation in the gut and lowered disease severity. The team also examined human MS tissue, finding increased TH17 cells and MHC II expression in intestinal epithelial cells. The findings were published in Science Immunology as “Intestinal Epithelial MHC Class II Induces Encephalitogenic CD4⁺ T Cells and Initiates Central Nerves System Autoimmunity,” pointing to intestinal immune education as a therapeutic site.