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γδ T cells play an essential role in the immune response to many pathogens, including  Plasmodium . However, long-lasting effects of infection on the γδ T cell population still remain inadequately understood. This study focused on assessing molecular and functional changes that persist in the γδ T cell population following resolution of malaria infection. We investigated transcriptional changes and memory-like functional capacity of malaria pre-exposed γδ T cells using a  Plasmodium   chabaudi  infection model. We show that multiple genes associated with effector function (chemokines, cytokines and cytotoxicity) and antigen-presentation were upregulated in  P. chabaudi -exposed γδ T cells compared to γδ T cells from naïve mice. This transcriptional profile was positively correlated with profiles observed in conventional memory CD8 +  T cells and was accompanied by enhanced reactivation upon secondary encounter with  Plasmodium -infected red blood cells  in vitro . Collectively our data demonstrate that  Plasmodium  exposure result in “memory-like imprints” in the γδ T cell population and also promotes γδ T cells that can support antigen-presentation during subsequent infections.

Transcriptional Memory-Like Imprints and Enhanced Functional Activity in γδ T Cells Following Resolution of Malaria Infection