SEMA4A and relapsing-remitting multiple sclerosis: Taken together, these observations support the possibility that Sema4A may facilitate disease onset of RRMS by promoting Th17 differentiation during the process of antigen-specific Th cell priming and furthermore may accelerate Th17 cell-mediated neuroinflammation in the effector phase, resulting in higher disease activity of patients with high Sema4A levels.