ATG5 in DCs attenuates anti-malarial cellular immune responses through interfering with TLR2-mediated CD209A/DC-SIGN expression

T cell responses. Furthermore, the expression of CD209A was mediated by the TLR2 (toll-like receptor 2) signaling pathway, which was significantly augmented in the absence of ATG5. Thus, we reveal a novel role for ATG5 in modulating anti-malarial cellular immune responses by influencing TLR2-mediated CD209A expression in cDCs. These findings not only enhance our understanding of impaired DC function during malaria infection but also provide valuable insights for the design of more effective malaria vaccines.