Polymorphisms in interferon regulatory factor 7 reduce interferon-α responses of plasmacytoid dendritic cells to HIV-1

被引：23

作者：

Chang, Judy ^{[1
]}

Lindsay, Robert J. ^{[1
]}

Kulkarni, Smita ^{[2
]}

Lifson, Jeffrey D. ^{[3
]}

Carrington, Mary ^{[1
,2
]}

Altfeld, Marcus ^{[1
]}

机构：

[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ragon Inst MGH MIT & Harvard, Boston, MA USA

[2] NCI, Canc & Inflammat Program, Expt Immunol Lab, Frederick, MD 21701 USA

[3] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21701 USA

来源：

AIDS | 2011年 / 25卷 / 05期

基金：

英国医学研究理事会; 美国国家卫生研究院;

关键词：

SIV INFECTION; IMMUNE ACTIVATION; VIRUS-INFECTIONS; NATURAL HOSTS; TLR7;

D O I：

10.1097/QAD.0b013e328343c186

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Recognition of HIV-1 ssRNA by Toll-like receptor 7 induces the production of the pro-inflammatory cytokines that may contribute to the systemic immune activation associated with HIV-1 disease progression. Here, we describe a novel association between polymorphisms in interferon regulatory factor 7 (IRF7), a master regulator of interferon-alpha (IFN-alpha), and the ability of plasmacytoid dendritic cells to produce IFN-alpha in response to HIV-1. IRF7 polymorphisms may, therefore, affect the ability of individuals to respond to HIV-1 and modulate HIV-1 disease progression.

引用

页码：715 / 717

页数：3

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