Delayed expansion of Vδ2⁺ and Vδ1⁺ γδ T cells after acute Plasmodium falciparum and Plasmodium vivax malaria

T lymphocytes that express T-cell receptors encoded by the γ and δ T-cell receptor genes (γδ T cells), and preferentially those expressing the Vγ9 and Vδ2 gene segments, are activated by microbial and parasitic organisms in vitro and have been implicated in the pathogenesis of the fever and rigors during acute malaria. We have found, in a cohort of nine nonimmune patients who contracted malaria during travel to endemic areas (five with Plasmodium falciparum and four with P. vivax infections) that γδ T lymphocytes expanded to comprise 17.92% ± 77% of the peripheral blood mononuclear cells (vs 3.08% ± 2.4% γδ cells in normal control subjects). Although Vδ2⁺ cells predominated among the γδ subset, γδ lymphocytes expressing the Vδ1 gene segment also expanded significantly in some patients. Importantly, the γδ cells continued to expand for 2 months after the infection, and the mean level of γδ cells peaked during the second month after the acute clinical syndrome, when patients were free of symptoms. Thus although γδ T cells may contribute to the pathogenesis of the acute clinical syndrome, our findings suggest that γδ lymphocytes could also play a role in generating an immune response to plasmodia.