The Role Of Mink1in Experimental Autoimmune Encephalomyelitis And Th17Cell Differentiation

Multiple sclerosis (MS) is an inflammatory autoimmune disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. The inflammatory process is basically caused by T helper17(Th17) cells. Here we demonstrate Mink1, a member of the germinal center kinase, is involved in the progression of experimental autoimmune encephalomyelitis (EAE), a disease model of MS. Mink1-/-mice developed severe autoimmune phenotype with induction of EAE. Meanwhile, we observed less naive T cell and more Th17differentiation in vitro in the presence of TGF-β and IL-6in Mink1-/-mice. Recently, Mink1was reported to inhibit TGF-β signaling by phosphorylating Smad. Our results indicate Mink1control autoimmunity via regulating Th17differentiation, probably through curbing the TGF-β signaling pathway.