CD86 and autoimmune disease: When DC‐T cell interactions occur without costimulatory signals (e.g., interactions with tolDC) or in an environment where signals suppress costimulation, T cells can lose their effector functions and become anergic.[29] Tolerogenic DC‐mediated peripheral tolerance is essential for preventing autoimmune diseases or hypersensitivity to antigens.[7] In this study, we observed that AE/M treatment downregulated the expression of CD86 and CD80 in splenic DC, promoting the induction of anergic T cells (Figure 7E–J).