In the study of EAE mouse model that simulates cllinical features of Multiple sclerosis (MS), IL-21R deletion caused a defect in IL-17-producing CD4+ T cell generation and limited IL-23R expression on Th17 cells, with reduction on the incidence and severity of spontaneous EAE, suggesting that IL-21/IL-21R signaling promotes pathogenic Th17 immune response and development of spontaneous disease [17]. Here, IL23R is linked to multiple sclerosis.