Keio University researchers linked intestinal epithelial cells to neuroinflammation in multiple sclerosis, reporting a mechanism in which IECs promote pathogenic TH17 T cell development that migrates to the spinal cord in mouse models. The study, published in Science Immunology, also analyzed human MS tissues and experimental autoimmune encephalomyelitis. Investigators found increased TH17 cells and upregulated MHC II expression in intestinal epithelial cells in both patients and the EAE model. Deleting MHC II in IECs reduced gut TH17 accumulation and lowered EAE severity, supporting a causal role for antigen presentation in the gut. The findings narrow future therapeutic targeting toward intestinal immunity by suggesting ways to modulate antigen-presenting activity or related pathways rather than focusing only on downstream CNS immune effects.