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. Here, CD4 is linked to autoimmune disease.