ATG5-regulated CCL2/MCP-1 production in myeloid cells selectively modulates anti-malarial CD4⁺ Th1 responses.

ABSTRACT: Parasite-specific CD4⁺ Th1 cell responses are the predominant immune effector for controlling malaria infection; however, the underlying regulatory mechanisms remain largely unknown. This study demonstrated that ATG5 deficiency in myeloid cells can significantly inhibit the growth of rodent blood-stage malarial parasites by selectively enhancing parasite-specific CD4⁺ Th1 cell responses. This effect was independent of ATG5-mediated canonical and non-canonical autophagy. Mechanistically, ATG5 deficiency suppressed FAS-mediated apoptosis of LY6G^- ITGAM/CD11b⁺ ADGRE1/F4/80^- cells and subsequently increased CCL2/MCP-1 production in parasite-infected mice. LY6G^- ITGAM⁺ ADGRE1^- cell-derived CCL2 selectively i

SUBMITTER: Gao Y 

PROVIDER: S-EPMC11210915 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature