gamma delta T cells contribute to control of chronic parasitemia in Plasmodium chabaudi infections in mice

During a primary infection of mice with Plasmodium chabaudi, gamma delta T cells are stimulated and their expansion coincides with recovery from the a cute phase of infection in normal mice or with chronic infections in B cell -deficient mice (mu-MT). To determine whether the large gamma delta T cell pool observed in female B cell-deficient mice is responsible for controllin g the chronic infection, studies were done using double-knockout mice defic ient in both B and gamma delta cells (mu-MT x delta(-/-)TCR) and in gamma d elta T cell-depleted mu-MT mice. In both types of gamma delta T cell-defici ent mice, the early parasitemia following the peak of infection was exacerb ated, and the chronic parasitemia was maintained at significantly higher le vels in the absence of gamma delta T cells. The majority of gamma delta T c ells in C57BL/6 and mu-MT mice responding to infection belonged predominant ly to a single family of gamma delta T cells with TCR composed of V gamma 2 V delta 4 chains and which produced IFN-gamma rather than IL-4.