ABSTRACT
J toxoplasma gondii establishes long-lasting asymptomatic infections in immunocompetent hosts including humans, but is an important opportunistic pathogen in immunocompromised patients or after transplacental transmission to fetuses. The abil ity to survive within hosts with an intact immune system relies on the parasite-mediated inhi bition of regulatory functions of macrophages, e.g., the downregulation of the M HC class II expression and the presentation o f antigens to CD4+ T lymphocytes. It is also facilitated by the downregulation of toxoplasmacidal effector functions of macrophages, e.g., the production of nitric oxide by the inducible nitric oxide synthase or the blockade of host cell apoptosis in parasite-infected cells. Progress that has been made in the characterization of the underlying molecular and cellular mechanisms reveals distinct interference by 77 gondii with signal trans duction cascades or other regulatory components of the host cell. These interactions provide fascinating examples of the elaborate mechanisms by which an intracellular parasite repro grams macrophages in order to establish chronic infection.
