Early changes in intestinal lymphoid and myeloid populations in experimental autoimmune encephalomyelitis.

Intestinal immunity is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes. Recent evidence also suggests its implication in the pathogenesis of autoimmune diseases affecting the central nervous system, such as multiple sclerosis (MS). However, there is ongoing debate regarding which part of the intestinal tract contributes to the development of MS. Therefore, our study aimed to explore the early changes in lymphoid and myeloid immune cells populations in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. We also sought to determine the roles of the colon and/or small intestine in the pathogenesis of EAE. By using flow cytometry, we revealed a transient increase in T and B lymphocytes in the ileal lamina propria of EAE mice just before the onset of motor symptoms. Additionally, we highlighted an increase in dendritic cells and monocytes/macrophages in the colonic lamina propria of EAE animals during the presymptomatic phase. Altogether, our findings indicate that both small intestine and colon are involved in the pathogenesis of EAE, despite engaging distinct immunological processes. This study provides new insights for understanding the roles of intestinal lymphoid and myeloid immune cells on the pathogenesis of MS and other autoimmune diseases.