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Modification of T-cell proliferation and interleukin 2 production in mice infected with Trypanosoma cruzi.
Author(s) -
Annick HarelBellan,
Miréille Joskowicz,
D Fradelizi,
Harvey Eisen
Publication year - 1983
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.80.11.3466
Subject(s) - concanavalin a , trypanosoma cruzi , interleukin 2 , immunology , biology , interleukin , immune system , spleen , chagas disease , interleukin 4 , population , cytokine , in vitro , medicine , parasite hosting , environmental health , world wide web , computer science , biochemistry
Acute infection of mice with Trypanosoma cruzi results in severe immunodepression and the appearance of autoimmune symptoms. In vitro, concanavalin A-stimulated T cells from spleens of infected animals could neither produce nor respond to interleukin 2. Interleukin 2 production was not restored by addition of exogenous interleukin 1, and proliferative response to concanavalin A was not restored by exogenous interleukin 2. A population of Thy-1-negative cells in the spleen of infected animals was shown to suppress the concanavalin A proliferative response and, to a lesser extent, the production of interleukin 2. These and other symptoms of T. cruzi-infected mice are similar to the immune dysfunction of autoimmune lpr/lpr mice. These findings are discussed in relationship to the pathology of Chagas disease.

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