Document Detail


Monocyte and macrophage dysfunction as a cause of HIV-1 induced dysfunction of innate immunity.
MedLine Citation:
PMID:  20937022     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
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.
Authors:
P Collini; M Noursadeghi; I Sabroe; R F Miller; D H Dockrell
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Current molecular medicine     Volume:  10     ISSN:  1875-5666     ISO Abbreviation:  Curr. Mol. Med.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-19     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101093076     Medline TA:  Curr Mol Med     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  727-40     Citation Subset:  IM    
Affiliation:
Department of Infection & Immunity, University of Sheffield, Sheffield, UK.
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Grant Support
ID/Acronym/Agency:
076945//Wellcome Trust; 077161//Wellcome Trust; 93762//Medical Research Council

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