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dc.contributor.authorHirsch, C. S.
dc.contributor.authorToossi, Z.
dc.contributor.authorJohnson, J. L.
dc.contributor.authorLuzze, H.
dc.contributor.authorNtambi, L.
dc.contributor.authorPeters, P.
dc.contributor.authorMcHugh, M.
dc.contributor.authorOkwera, A.
dc.contributor.authorJoloba, M.
dc.contributor.authorMugyenyi, P.
dc.contributor.authorMugerwa, R. D.
dc.contributor.authorTerebuh, P.
dc.contributor.authorEllner, J. J.
dc.date.accessioned2013-03-01T07:26:54Z
dc.date.available2013-03-01T07:26:54Z
dc.date.issued2001-02-08
dc.identifier.citationThe Journal of Infectious Diseases 2001; 183:779–788en_US
dc.identifier.issn0022-1899
dc.identifier.urihttp://hdl.handle.net/123456789/519
dc.identifier.urihttp://www.journals.uchicago.edu/toc/jid/current
dc.identifier.urihttp://hdl.handle.net/10570/1161
dc.description© 2001 by The Infectious Diseases Society of America. This article can be accessed from http://www.journals.uchicago.edu/toc/jid/currenten_US
dc.description.abstractPleural tuberculosis (TB) was employed as a model to study T cell apoptosis at sites of active Mycobacterium tuberculosis (MTB) infection in human immunodeficiency virus (HIV)–coinfected (HIV/TB) patients and patients infected with TB alone. Apoptosis in blood and in pleural fluid mononuclear cells and cytokine immunoreactivities in plasma and in pleural fluid were evaluated. T cells were expanded at the site of MTB infection, irrespective of HIV status. Apoptosis of CD4 and non-CD4 T cells in the pleural space occurred in both HIV/TB and TB. Interferon (IFN)–g levels were increased in pleural fluid, compared with plasma. Spontaneous apoptosis correlated with specific loss of MTB-reactive, IFN-g–producing pleural T cells. Immunoreactivities of molecules potentially involved in apoptosis, such as tumor necrosis factor–a, Fas-ligand, and Fas, were increased in pleural fluid, compared with plasma. These data suggest that continued exposure of immunoreactive cells to MTB at sites of infection may initiate a vicious cycle in which immune activation and loss of antigenresponsive T cells occur concomitantly, thus favoring persistence of MTB infection.en_US
dc.language.isoenen_US
dc.publisherUniversity of Chicago Pressen_US
dc.subjectMycobacterium tuberculosisen_US
dc.subjectHuman tuberculosisen_US
dc.titleAugmentation of Apoptosis and Interferon-g Production at sites of active Mycobacterium Tuberculosis infection in Human Tuberculosisen_US
dc.typeConference paperen_US


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