Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are neuroinflammatory autoimmune diseases characterized by the axonal loss, demyelination, and neurodegeneration of the central nervous system. Overactivation of CD4+ T cells, especially the migration of the Th1 and Th17 subsets into the central nervous system (CNS), leads to the secretion of inflammatory mediators and destruction of the contact between neurons and activated macrophages, which can then result in a series of neurocognitive and motor deficits. In this study, we intended to explore the role of miRNA-467b in regulating Th cell development in EAE. We found that the level of miRNA-467b was decreased and eukaryotic initiation factor 4 F (eIF4E) was increased in lymph nodes and the CNS at EAE peak. eIF4E was confirmed as the direct target of miRNA467b. Overexpression of miRNA-467b could suppress a percentage of CD4+ IL-17+ cells in EAE CD4 + T cells in vitro. In addition, we also identified miRNA-467b, which could suppress Th17 cell differentiation by targeting eIF4E in vitro. Furthermore, injecting miRNA-467b mimics into the caudal vein of EAE mice contributed to less inflammation in the peripheral lymphoid organs and CNS and alleviated disease severity. Taken together, our findings imply that miRNA-467b inhibits the differentiation and function of Th17 cells by targeting eIF4E, thereby alleviating EAE.