γδ T Cells Contribute to Control of Chronic Parasitemia in Plasmodium chabaudi Infections in Mice

During a primary infection of mice with Plasmodium chabaudi, γδ T cells are stimulated and their expansion coincides with recovery from the acute phase of infection in normal mice or with chronic infections in B cell-deficient mice (μ-MT). To determine whether the large γδ T cell pool observed in female B cell-deficient mice is responsible for controlling the chronic infection, studies were done using double-knockout mice deficient in both B and γδ cells (μ-MT × δ−/−TCR) and in γδ T cell-depleted μ-MT mice. In both types of γδ T cell-deficient mice, the early parasitemia following the peak of infection was exacerbated, and the chronic parasitemia was maintained at significantly higher levels in the absence of γδ T cells. The majority of γδ T cells in C57BL/6 and μ-MT mice responding to infection belonged predominantly to a single family of γδ T cells with TCR composed of Vγ2Vδ4 chains and which produced IFN-γ rather than IL-4.