Transcriptional memory-like imprints and enhanced functional activity in gamma delta T cells following resolution of malaria infection

Gamma delta T cells play an essential role in the immune response to many pathogens, including Plasmodium. However, long-lasting effects of infection on the gamma delta T cell population still remain inadequately understood. This study focused on assessing molecular and functional changes that persist in the gamma delta T cell population following resolution of malaria infection. We investigated transcriptional changes and memory-like functional capacity of malaria pre-exposed gamma delta 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 gamma delta T cells compared to gamma delta T cells from naive 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 gamma delta T cell population and also promotes gamma delta T cells that can support antigen-presentation during subsequent infections

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

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