The obligate intracellular protozoan pathogen Toxoplasma gondii is estimated to infect a third of the world's population. Toxoplasmosis is considered a significant worldwide disease that can lead to morbidity or death in immunocompromised individuals. Host defense against T. gondii has been demonstrated to be dependent on a rapid myeloid cell and lymphocyte response working in concert to quickly eliminate the invading pathogen. Classically, T-bet-dependent group 1 innate lymphocytes (ILC1s), natural killer (NK) cells, and CD4+ T cell-derived interferon-γ (IFN-γ) are considered indispensable for host resistance against T. gondii. However, recent discoveries have illustrated that T-bet is not required for NK cell- or CD4+ T cell-derived IFN-γ. Yet, lack of T-bet still results in rapid mortality, pointing to a T-bet-dependent myeloid cell-mediated host defense pathway. This review summarizes the myeloid cell-mediated immune response against T. gondii and provides insights into the lesser known components of the T-bet-dependent myeloid cell-dependent host defense pathway for pathogen clearance.
Schanz et al. (Mon,) studied this question.