title: Immunopathogenesis of cerebral toxoplasmosis.
abstract: Interferon (IFN)-gamma is an absolute requirement for resistance against acute acquired infection with Toxoplasma gondii and development of toxoplasmic encephalitis (TE) during the late stage of infection. Multiple populations of both T and non-T cells are important sources of IFN-gamma in resistance. In the absence of IFN-gamma-producing non-T cells, T cells cannot prevent TE. Interleukin-12, Bcl-3, NF-kappaB(2), and CD40-CD40L ligand interaction are important for up-regulation of IFN-gamma production. T. gondii infects a variety of host cells, and IFN-gamma-mediated immune responses control the parasite in both phagocytic and nonphagocytic cells through at least five different mechanisms, most likely depending on the types of cells responding to IFN-gamma. Such effector functions involve production of NO by iNOS, tryptophan degradation by the enzyme IDO (indolamine 2,3-dioxygenase), unidentified mechanism(s) mediated by 47- to 48-kDa proteins encoded by an IFN-gamma responsive gene family, limiting the availability of intracellular iron to the parasite, and production of reactive oxygen intermediates.
authors.affiliation: Center for Molecular Medicine/Infectious Diseases, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, 1410 Prices Fork Road, Blacksburg, VA 24061, USA. ysuzuki@vt.edu
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D004660:Encephalitis / Q000276:immunology* / Q000469:parasitology / Q000503:physiopathology*; D006801:Humans; D007111:Immunity, Cellular; D007371:Interferon-gamma / Q000096:biosynthesis; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D014122:Toxoplasma / Q000276:immunology; D016781:Toxoplasmosis, Cerebral / Q000276:immunology* / Q000469:parasitology / Q000503:physiopathology*
chemical_list: D007371:Interferon-gamma