IBCB Scientists Found the Regulatory Mechanism of a MicroRNA in Multiple Sclerosis

MS is a complicated human autoimmune disease that damages the central nervous system (CNS), counting for one of the foremost causes of non-traumatic neurological disability in young adults and still lacking effective approaches for clinical therapy. Studies in recent years have shown that the Interleukin (IL)-17 producing CD4+ T cells, namely the TH-17 cells, are potently induced in variety of autoimmune diseases and can actively penetrate into the CNS of MS patients, leading to demyelination and CNS tissue damages.

Thus, a comprehensive understanding of the molecular mechanism regulating the differentiation of TH-17 cells is of great importance for the treatment of MS.

Latest results from a SIBCB group led by Prof. PEI Gang, a CAS Member, offers new diagnosis and therapeutic strategy for MS. Gang Pei and his colleagues found that a non-coding microRNA (miR-326) whose expression is up-regulated in the CD4+ T cells of MS patients and positively correlates with the IL-17 levels.

They proved in the experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, that in vivo silencing of miR-326 resulted in fewer TH-17 cells and mild EAE, and its overexpression led to more TH-17 cells and severe EAE. Their mechanistic study demonstrated that miR-326 promoted the differentiation of TH-17 cells by inhibition of Ets-1 expression, a negative transcription regulator of TH-17 differentiation.