ATG5-Regulated CCL2/MCP-1 Production in Myeloid Cells Selectively Modulates Anti-malarial CD4+ Th1 Responses

Researchers 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.