Induction of γδ T cells during acute murine infection with Toxoplasma gondii

Abstract

Abstract The importance of the host γδ T cell response to microbial pathogens is not yet fully understood. We report that inbred mice infected with T. gondii developed a γδ T cell proliferative response to parasite Ag. Mice depleted of either the αβ or γδ TCR were found to be significantly more susceptible to infection than the parent mouse strain. Proliferation of γδ T cells was observed in mice deficient in the TCR-αβ in response to UV-irradiated parasites. These T cells lyse parasite-infected syngenic macrophages. Adoptive transfer of these γδ T cells into β2 microglobulin-deficient mice that have been depleted of both CD4+ and NK cells prolongs survival against acute parasite challenge when compared with nontransferred controls. The γδ T cells isolated from infected α -/- mice express a 10-fold increase in mRNA and produce high titers of IFN-γ. These data suggest that γδ T cells may play an important role in the early host response to infection with T. gondii.