Our present study demonstrated that Optn deficiency hampered the antigen presenting function of DCs and their ability to activate CD4+ T cells and differentiate into Th1 and Th17 subtypes, and Optn conditional knockout via CD11c-Cre in mice model could effectively disrupt the progression of EAE, a T cells dependent experimental autoimmune disease (Supplementary Fig. 8). This evidence concerns the gene ITGAX and autoimmune disease.