c mice (original) (raw)

Many different cell populations or lineages participate in the resistance to Trypanosoma cruzi infection. gd T cells may also take part in a network of interactions that lead to control of T. cruzi infection with minimal tissue damage by controlling ab T cell activation, as was previously suggested. However, the gd T cell population is not homogeneous and its functions might vary, depending on T cell receptor usage or distinct stimulatory conditions. In this study, we show that the in vivo depletion of Vg1-bearing gd T cells, prior to the infection of BALB/c mice with the Y strain of T. cruzi, induces an increased susceptibility to the infection with lower amounts of IFN-g being produced by conventional CD4þ or CD8þ T cells. In addition, the production of IL-4 by spleen T cells in Vg1-depleted mice was increased and the production of IL-10 remained unchanged. Since Vg1 þ gd T cell depletion diminished the conversion of naive to memory/activated CD4 T cells and the production of IFN-g during the acute infection, these cells appear to function as helper cells for conventional CD4þ Th1 cells. Depletion of Vg1 þ cells also reduced the infection-induced inflammatory infiltrate in the heart and skeletal muscle. More importantly, Vg1 þ cells were required for up-regulation of CD40L in CD4þ and CD8þ T cells during infection. These results show that a subset of gd T cells (Vg1 þ), which is an important component of the innate immune response, up-regulates the type 1 arm of the adaptative immune response, during T. cruzi infection.