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The Journal of Immunology, 1999, 162: 2837-2841.
Copyright © 1999 by The American Association of Immunologists

{gamma}{delta} T Cells Contribute to Control of Chronic Parasitemia in Plasmodium chabaudi Infections in Mice1

Elsa M. G. Seixas and Jean Langhorne2

Department of Biology, Imperial College of Science, Technology and Medicine, London, U.K.

During a primary infection of mice with Plasmodium chabaudi, {gamma}{delta} 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 {gamma}{delta} 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 {gamma}{delta} cells (µ-MT x {delta}-/-TCR) and in {gamma}{delta} T cell-depleted µ-MT mice. In both types of {gamma}{delta} 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 {gamma}{delta} T cells. The majority of {gamma}{delta} T cells in C57BL/6 and µ-MT mice responding to infection belonged predominantly to a single family of {gamma}{delta} T cells with TCR composed of V{gamma}2V{delta}4 chains and which produced IFN-{gamma} rather than IL-4.




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