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Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/519

Title: Augmentation of Apoptosis and Interferon-g Production at sites of active Mycobacterium Tuberculosis infection in Human Tuberculosis
Authors: Hirsch, C. S.
Toossi, Z.
Johnson, J. L.
Luzze, H.
Ntambi, L.
Peters, P.
McHugh, M.
Okwera, A.
Joloba, M.
Mugyenyi, P.
Mugerwa, R. D.
Terebuh, P.
Ellner, J. J.
Keywords: Mycobacterium tuberculosis
Human tuberculosis
Issue Date: 8-Feb-2001
Publisher: University of Chicago Press
Citation: The Journal of Infectious Diseases 2001; 183:779–788
Abstract: Pleural 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.
Description: © 2001 by The Infectious Diseases Society of America. This article can be accessed from http://www.journals.uchicago.edu/toc/jid/current
URI: http://www.journals.uchicago.edu/toc/jid/current
http://hdl.handle.net/123456789/519
ISSN: 0022-1899
Appears in Collections:Research Articles (Bio-Medical)

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