ATG5 controls CD80 expression in B cells and shapes cognate CD4⁺ T cell responses.

ABSTRACT: The macroautophagy/autophagy machinery has been implicated in supporting MHC class II but compromising MHC class I restricted antigen presentation by dendritic cells (DCs). Here, we report that loss of the essential autophagy protein ATG5 in B cells reduces internalization and stabilizes co-stimulatory CD80 surface expression. In an adjuvant-free experimental autoimmune encephalomyelitis (EAE) mouse model, co-transfer of MOG-specific induced germinal center B (iGB) cells deficient in ATG5 with MOG-specific CD4⁺ T cells, accelerated disease development. CD80 blockade abrogated enhanced cognate CD4⁺ T-cell responses induced by iGB cells lacking ATG5. These data broaden the concept of ATG5-mediated antigen presentation and indicate that ATG5 might not only enhance, as de

SUBMITTER: Passos I 

PROVIDER: S-EPMC12459358 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature