A Keio University-led study identified a gut-immune mechanism that can initiate neuroinflammation in multiple sclerosis models. Researchers reported that intestinal epithelial cells (IECs) with upregulated MHC class II promote the development of pathogenic TH17 cells that migrate to the spinal cord and drive disease symptoms in mouse models. The team examined intestinal tissue from MS patients and from mice with experimental autoimmune encephalomyelitis (EAE), reporting increases in TH17 cells and MHC II expression in IECs in both settings. In a key mechanistic step, deleting MHC II in IECs reduced TH17 accumulation in the gut and lowered EAE severity. The findings were published in Science Immunology in a paper titled “Intestinal Epithelial MHC Class II Induces Encephalitogenic CD4⁺ T Cells and Initiates Central Nerves System Autoimmunity.” The authors said the work could inform targeted therapeutics that modulate intestinal antigen presentation rather than focusing only on B cells. For biotech stakeholders in autoimmune neurology, the study expands the therapeutic target set to gut-resident immune education pathways, potentially enabling new drug development programs aimed at local immune modulation.