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American Journal of Pathology, Vol 146, 999-1007, Copyright © 1995 by American Society for Investigative Pathology
REGULAR ARTICLES |
D Schluter, A Hein, R Dorries and M Deckert-Schluter
Department of Medical Microbiology and Hygiene, Heidelberg University, Mannheim Clinic, Germany.
Oral infection of athymic nude and immunocompetent Lewis rats with Toxoplasma gondii induced a chronic nonlethal encephalitis. The histopathological pattern of Toxoplasma encephalitis was significantly different in both groups of animals and there were substantially larger numbers of Toxoplasma cysts in the brains of athymic rats. Combined immunohistochemical and flow cytometric analyses of intracerebral leukocytes identified alpha beta TCR+ CD4+ and CD8+ T cells; macrophages, and natural killer cells as inflammatory cell populations in immunocompetent rats, whereas in athymic rats natural killer cells, macrophages, and gamma delta TCR+ CD8+ CD3+ T cells contributed to the intracerebral inflammatory infiltrates. These findings not only point to a major participation of alpha beta TCR+ T cells to the intracerebral immune response, but also indicate that they are not essential to prevent the development of a lethal Toxoplasma encephalitis. In addition, microglia were strongly activated in both strains with simultaneous up-regulation of major histocompatibility complex class I and II antigens and CD4. Activation of microglia was most prominent in athymic rats, demonstrating that immunodeficiency does not preclude an up-regulation of these molecules including the human immunodeficiency virus receptor CD4 on microglial cells.
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