Severe malaria enforces short-lived effector cell differentiation but does not prevent effective secondary responses by memory CD8 T cells.

ABSTRACT: Parasitic infections are a major worldwide health burden, yet most studies of CD8 T cell differentiation focus on acute viral and bacterial infections. To understand effector and memory CD8 T cell responses during erythrocytic malaria infection in mice, we utilized transgenic OT-I T cells and compared CD8 T cell responses between infection with OVA-expressing strains of Listeria monocytogenes (Lm) and Plasmodium berghei ANKA (PbA). We find that CD8 T cells expand vigorously during both infections. However, in contrast to Lm infection, PbA infection induces T cells that are heavily biased toward an IL-7Ra-deficient and KLRG1+ short-lived effector cell (SLEC) phenotype at the expense of memory precursor effector cell (MPECs) formation. PbA-induced inflammation, including IFNγ, is partially r

SUBMITTER: Hildebrand JA 

PROVIDER: S-EPMC11957282 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature