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Monocyte and macrophage dysfunction as a cause of HIV-1 induced dysfunction of innate immunity

Collini, P., Noursadeghi, M., Sabroe, I., Miller, R. F. and Dockrell, D. H. (2010) Monocyte and macrophage dysfunction as a cause of HIV-1 induced dysfunction of innate immunity. Current molecular medicine, 10 (8). pp. 727-40. ISSN 1875-5666

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Abstract

HIV-1 can establish both long lived and productive infection of macrophages (Mϕ) but circulating monocytes are less permissive to infection. Multiple studies have identified extensive changes to monocyte and Mϕ phenotype, differentiation or function. These include alterations in Toll-like receptor signaling and resultant changes to cytokine responses, specific defects in phagocytosis and microbial killing and modulation of apoptotic responses, all of which may perturb the important role of these cells in innate immunity. Interpretation of contradictory data however, is complicated by the use of different experimental models and many of the reported effects may be an indirect consequence of HIV 1 infection that result from exposure to viral products or from disruption of cellular and cytokine networks in the immune system, rather than the direct consequence of productive HIV 1 infection. Future research should focus on refining experimental models and on elucidating the physiological mechanisms of monocyte/ Mϕ dysfunction during HIV 1 infection.

Item Type: Article
Keywords: Apoptosis, HIV-1, innate immunity, macrophage, monocyte, phagocytosis, Lentiviruses, Maedi-visna, antiretroviral therapy, immunoreactive factors, replication, viremia, monocytes, transcription, SIV infection, encephalopathy, polarization, Mycobacterium tuberculosis
Academic Units: The University of Sheffield > Faculty of Medicine, Dentistry and Health (Sheffield) > School of Medicine (Sheffield) > Department of Infection & Immunity
Depositing User: Miss Anthea Tucker
Date Deposited: 29 Mar 2012 09:55
Last Modified: 29 Mar 2012 09:55
Published Version: http://dx.doi.org/10.2174/156652410793384141
Status: Published
Publisher: Bentham Science Publishers
Identification Number: 10.2174/156652410793384141
Related URLs:
URI: http://eprints.whiterose.ac.uk/id/eprint/43794

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