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|Title: ||Augmentation of Apoptosis and Interferon-g Production at sites of active Mycobacterium Tuberculosis infection in Human Tuberculosis|
|Authors: ||Hirsch, C. S.|
Johnson, J. L.
Mugerwa, R. D.
Ellner, J. J.
|Keywords: ||Mycobacterium 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|
|Appears in Collections:||Research Articles (Bio-Medical)|
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