Multiple sclerosis (MS) is a debilitating neurological disorder caused by malfunctioning immune responses that target the brain and spinal cord of the central nervous system (CNS). New research led by Shohei Suzuki, MD, PhD, assistant professor, division of gastroenterology and hepatology, and Tomohisa Sujino, PhD, associate professor, School of Medicine, at Keio University, Japan, has now indicated how the gut can initiate neuroinflammation in multiple sclerosis. Their study found that intestinal epithelial cells (IECs) promote the development of pathogenic T cells that migrated to the spinal cord and induced disease symptoms in mouse models of the disorder. The researchers examined intestinal tissues from patients with MS and mice with experimental autoimmune encephalomyelitis (EAE), a close analog of MS. In both cases, they observed an increase in TH17 cells and an upregulation of major histocompatibility complex class II (MHC II) expression in IECs. Deleting MHC II in IECs reduced the accumulation of TH17 cells in the gut and lowered the severity of EAE. They suggest the results could inform future strategies for developing targeted therapeutics against autoimmunity. “While current therapies for MS often target B cells, our study highlights the gut as an important therapeutic site,” Suzuki commented. “Modulating intestinal microbiota or antigen-presenting activity of IECs represents new approaches to treating autoimmune neurological diseases.” Suzuki, Sujino, and colleagues reported on their findings in Science Immunology, in a paper titled “Intestinal Epithelial MHC Class II Induces Encephalitogenic CD4⁺ T Cells and Initiates Central Nerves System Autoimmunity,” in which they concluded, “Our findings…
