MicroRNAs and their Implications in CD4+ T-cells, Oligodendrocytes and Dendritic Cells in Multiple Sclerosis Pathogenesis

Abstract

Abstract: MicroRNAs (miRNAs) have been established as key players in various biological processes regulating differentiation, proliferation, inflammation, and autoimmune disorders. Emerging evidence suggests the critical role of miRNAs in the pathogenesis of multiple sclerosis (M.S.). Here, we provide a comprehensive overview on miRNAs which are differentially expressed in M.S. patients or experimental autoimmune encephalomyelitis (EAE) mice and contribute to M.S. pathogenesis through regulating diverse pathways including CD4+ T cells proliferation, differentiation, and activation in three subtypes of CD4+ T cells including Th1, Th17 and regulatory T cells (Tregs). Moreover, regulation of oligodendrocyte precursor cells (OPC) differentiation as a crucial player of M.S. pathogenesis is also described. Our literature research showed that miR-223 could affect different pathways involved in M.S. pathogenesis, such as promoting Th1 differentiation, activating the M2 phenotype of myeloid cells, and clearing myelin debris. MiR-223 was also identified as a potential biomarker, distinguishing relapsing-remitting multiple sclerosis (RRMS) from progressive multiple sclerosis (PMS), and thus, it may be an attractive target for further investigations. Our overview provides a novel, potential therapeutic targets for the treatment and new insights into miRNAs' role in M.S. pathogenesis.