Plasmodium berghei XAT: Contribution of γδ T cells to host defense against infection with blood-stage nonlethal malaria parasite

We examined a potential role of γδ T cells in protective immunity to blood-stage Plasmodium berghei XAT infection. Plasmodium berghei XAT is an attenuated variant of the lethal strain P. berghei NK65 and its infection is self-resolving in immune competent mice. To determine whether γδ T cells are essential for the resolution of P. berghei XAT malaria, mice were depleted of γδ T cells with anti-TCRγδ antibody treatment. Although mice that had received control antibody resolved infections, mice received anti-TCRγδ antibody could not control their infections and eventually died. Spleen cells from infected mice produced IFN-γ and nitric oxide (NO) within the first week of infection, however, levels of IFN-γ and NO in γδ T cell-depleted mice were significantly lower than in control mice. To examine whether γδ T cells are involved in the antibody production, malarial-specific antibodies of the various isotypes were measured in the sera of γδ T cell-depleted mice and control mice. Serum levels of IgG2a, which was known to be a protective antibody in P. berghei XAT malaria, were significantly lower in γδ T cell-depleted mice than in control mice, whereas levels of IgG1 were comparable to those in control mice. Our results indicated that the presence of the γδ T cell subset was essential for resolution of blood-stage P. berghei XAT malaria and played a modulatory role in the development of Th1 response and host defense against this malarial parasites.