HLA Class I Subtype-Dependent Expansion of KIR3DS1+ and KIR3DL1+ NK Cells during Acute Human Immunodeficiency Virus Type 1 Infection

被引：151

作者：

Alter, Galit ^{[1
,2
,3
]}

Rihn, Suzannah ^{[1
,2
,3
]}

Walter, Katharine ^{[1
,2
,3
]}

Nolting, Anne ^{[1
,2
,3
]}

Martin, Maureen ^{[4
]}

Rosenberg, Eric S. ^{[1
,2
,3
]}

Miller, Jeffrey S. ^{[5
]}

Carrington, Mary ^{[4
]}

Altfeld, Marcus ^{[1
,2
,3
]}

机构：

[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Infect Dis Unit, Boston, MA 02129 USA

[2] Harvard Univ, Ragon Inst MGH MIT & Harvard, Sch Med, Boston, MA 02129 USA

[3] Harvard Univ, Div AIDS, Sch Med, Boston, MA 02129 USA

[4] SAIC Frederick Inc, Basic Res Program, Lab Genom Div, Frederick, MD USA

[5] Univ Minnesota, Ctr Canc, Div Hematol Oncol & Transplantat, Minneapolis, MN USA

来源：

JOURNAL OF VIROLOGY | 2009年 / 83卷 / 13期

基金：

美国国家卫生研究院;

关键词：

NATURAL-KILLER-CELLS; IMMUNOGLOBULIN-LIKE RECEPTOR; ACUTE HIV-1 INFECTION; INHIBITORY RECEPTORS; PERIPHERAL-BLOOD; SELF-MHC; INNATE; CYTOMEGALOVIRUS; ACTIVATION; RESISTANCE;

D O I：

10.1128/JVI.00256-09

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

NK cells are critical in the early containment of viral infections. Epidemiological and functional studies have shown an important role of NK cells expressing specific killer immunoglobulin-like receptors (KIRs) in the control of human immunodeficiency virus type 1 (HIV-1) infection, but little is known about the mechanisms that determine the expansion of these antiviral NK cell populations during acute HIV-1 infection. Here we demonstrate that NK cells expressing the activating receptor KIR3DS1(+) and, to a lesser extent, the inhibitory receptor KIR3DL1(+) specifically expand in acute HIV-1 infection in the presence of HLA-B Bw480I, the putative HLA class I ligand for KIR3DL1/3DS1. These data demonstrate for the first time the HLA class I subtype-dependent expansion of specific KIR+ NK cells during an acute viral infection in humans.

引用

页码：6798 / 6805

页数：8

共 37 条

[1] Sequential deregulation of NK cell subset distribution and function starting in acute HIV-1 infection [J].