Keio University researchers identified a mechanistic gut-immune link in multiple sclerosis-related neuroinflammation, reporting that intestinal epithelial cells promote development of pathogenic T cells that drive central nervous system autoimmunity. Led by Shohei Suzuki, MD, PhD, and Tomohisa Sujino, PhD, the team found increased TH17 cells and upregulated MHC class II expression in intestinal epithelial cells from patients with MS and from mice with experimental autoimmune encephalomyelitis. In mouse models, deleting MHC II in intestinal epithelial cells reduced TH17 accumulation in the gut and lowered EAE severity. The work, published in Science Immunology, suggests that intestinal immune education and antigen presentation could be leveraged for targeted autoimmune therapies. For biopharma, the implication is a new tissue-level immunology target that complements existing MS strategies focused elsewhere in the immune system.