In addition, we also observed that TLR2s on T cells were involved in the IL-17A response, which was consistent with Joseph Reynolds’s study: TLR2 agonists activated TLR2 signaling in CD4 + T cells and led to more robust proliferation and TH17 cytokine production, resulting in more severe pathology in autoimmune diseases such as EAE19. This evidence concerns the gene IL17A and autoimmune disease.