Clinical Microbiology Reviews, October 1998, p. 569-588, Vol. 11, No. 4
Department of Microbiology and Immunology,
College of Veterinary Medicine, Cornell University, Ithaca, New
York 14853-6401,1 and
Department of
Biochemistry and Immunology, Federal University of Minas Gerais,
Belo Horizonte 30161-970, MG, Brazil2
The intracellular protozoan Toxoplasma gondii is a widespread opportunistic parasite of humans and animals. Normally, T. gondii establishes itself within brain and skeletal muscle tissues, persisting for the life of the host. Initiating and sustaining strong T-cell-mediated immunity is crucial in preventing the emergence of T. gondii as a serious pathogen. The parasite induces high levels of gamma interferon (IFN-
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Regulation and Function of T-Cell-Mediated Immunity
during Toxoplasma gondii Infection
) during initial infection as a result of early T-cell as well as natural killer (NK) cell activation. Induction of interleukin-12 by macrophages is a major mechanism driving early IFN-
synthesis. The latter cytokine, in addition to promoting the differentiation of Th1 effectors, is important in macrophage activation and acquisition of microbicidal functions, such as nitric oxide release. During chronic infection, parasite-specific T lymphocytes release high levels of IFN-
, which is required to prevent cyst reactivation. T-cell-mediated cytolytic activity against infected cells, while easily demonstrable, plays a secondary role to inflammatory cytokine production. While part of the clinical manifestations of toxoplasmosis results from direct tissue destruction by the parasite, inflammatory cytokine-mediated immunopathologic changes may also contribute to disease progression.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853-6401. Phone: (607) 253-4022. Fax: (607)
253-3384. E-mail: eyd1{at}cornell.edu.
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