Document Detail


Human immunodeficiency virus type 1 Nef in human monocyte-like cell line THP-1 expands Treg cells via Toll-like receptor 2.
MedLine Citation:
PMID:  21845735     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
CD4(+) CD25(+) regulatory T cells (Tregs) represent a unique T-cell lineage that is endowed with the ability to actively suppress immune responses in order to inhibit pathogenic damage resulting from over activation of the immune system. In human immunodeficiency virus-1 (HIV-1) infection, suppression of the immune response by Tregs appears to play an opposing role that promotes chronic viral infection. Treg expansion is known as a marker of the severity of HIV infection and as a potential prognostic marker of disease progression. HIV-1 Nef is one of the earliest expressed viral regulatory genes whose expression may play an important role in regulating Treg cells. We established a THP-1 cell line stably expressing HIV-1 Nef and showed that Nef protein was a potent factor for increasing Treg numbers in vitro. We further found that TLR2 plays a critical role in the increase in Treg cells induced by Nef using TLR2-specific siRNA. Our results suggest new strategies for therapeutic and preventive interventions of HIV infection. J. Cell. Biochem. © 2011 Wiley-Liss, Inc.
Authors:
Xiaolin Qin; Jiahong Yao; Fan Yang; Jiqin Nie; Yanlin Wang; Chaoqi Liu
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-8-15
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  -     ISSN:  1097-4644     ISO Abbreviation:  -     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-8-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011 Wiley-Liss, Inc.
Affiliation:
Institute of Molecular Biology of Three Gorges University, Yichang 443002, Hubei Province, P.R.China.
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