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Apoptotic cell death in the pathogenesis of infectious diseases

Dockrell, D. H. (2001) Apoptotic cell death in the pathogenesis of infectious diseases. The Journal of infection, 42 (4). pp. 227-234. ISSN 0163-4453

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Abstract

Apoptosis is a physiological process critical for tissue homeostasis. It is essential for the regulation of immune responses. A series of molecules transduce apoptoic signals and induce the characteristic morphological appearances of apoptotic cells. Infectious diseases modulate apoptosis and this contributes to disease pathogenesis. Infection with HIV results in enhanced levels of CD4 T-lymphocyte apoptosis in both directly infected cells and in uninfected bystander cells. A variety of HIV proteins including gp120 contribute to this process. A number of different pathways induce HIV-associated CD4 T-lymphocyte apoptosis and apoptosis of uninfected bystander cells is particularly associated with increased susceptibility to Fas. Other viruses including hepatitis viruses and the human herpesviruses also modulate apoptosis. Bacterial infection induces apoptosis which is frequently mediated by the direct activation of caspases in the absence of death receptor ligation. Bacterial induction of apoptosis may either be due to bacterial factors such as the invasin IpaB of Shigella flexneri or be the result of host immune responses which control infection as demonstrated in infections due to Mycobacterium spp. Apoptosis may be modulated by therapeutic strategies, such as antiretroviral therapy, and an improved understanding of infection-associated apoptosis modulation will aid the design of novel therapeutic approaches to control infectious diseases.

Item Type: Article
Academic Units: The University of Sheffield > Faculty of Medicine, Dentistry and Health (Sheffield) > School of Medicine (Sheffield)
Depositing User: Miss Anthea Tucker
Date Deposited: 29 Mar 2012 09:44
Last Modified: 29 Mar 2012 09:44
Published Version: http://dx.doi.org/10.1053/jinf.2001.0836
Status: Published
Publisher: Elsevier
Identification Number: 10.1053/jinf.2001.0836
Related URLs:
URI: http://eprints.whiterose.ac.uk/id/eprint/43823

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