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Clinical and Developmental Immunology
Volume 2011 (2011), Article ID 678570, 11 pages
Review Article

Modulation of Cell Death by M. tuberculosis as a Strategy for Pathogen Survival

1Armauer Hansen Research Institute, P.O. Box 1005, Addis Ababa, Ethiopia
2The Centre for Infectious Diseases and International Health, Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, London WC1T 4JF, UK
3Department of Infectious Disease Immunology, Statens Serum Institute, Artillerivej 5, København S, 2300 Copenhagen, Denmark

Received 17 September 2010; Accepted 27 November 2010

Academic Editor: Nicholas West

Copyright © 2011 Markos Abebe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It has been clearly demonstrated that in vitro, virulent M. tuberculosis can favor necrosis over apoptosis in infected macrophages, and this has been suggested as a mechanism for evading the host immune response. We recently reported that an effect consistent with this hypothesis could be observed in cells from the blood of TB patients, and in this paper, we review what is known about evasion strategies employed by M. tuberculosis and in particular consider the possible interaction of the apoptosis-inhibiting effects of M. tuberculosis infection with another factor (IL-4) whose expression is thought to play a role in the failure to control M. tuberculosis infection. It has been noted that IL-4 may exacerbate TNF-α-induced pathology, though the mechanism remains unexplained. Since pathology in TB typically involves inflammatory aggregates around infected cells, where TNF-α plays an important role, we predicted that IL-4 would inhibit the ability of cells to remove M. tuberculosis by apoptosis of infected cells, through the extrinsic pathway, which is activated by TNF-α. Infection of human monocytic cells with mycobacteria in vitro, in the presence of IL-4, appears to promote necrosis over apoptosis in infected cells—a finding consistent with its suggested role as a factor in pathology during M. tuberculosis infection.