Intact NKG2D-Independent Function of NK Cells Chronically Stimulated with the NKG2D Ligand Rae-1

被引：33

作者：

Champsaur, Marine ^{[1
,2
]}

Beilke, Joshua N. ^{[1
,2
]}

Ogasawara, Kouetsu ^{[1
,2
]}

Koszinowski, Ulrich H. ^{[4
]}

Jonjic, Stipan ^{[3
]}

Lanier, Lewis L. ^{[1
,2
]}

机构：

[1] Univ Calif San Francisco, Dept Microbiol & Immunol, Biomed Sci Grad Program, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Canc Res Inst, San Francisco, CA 94143 USA

[3] Univ Rijeka, Sch Med, Rijeka, Croatia

[4] Max Von Pettenkofer Inst, Munich, Germany

来源：

JOURNAL OF IMMUNOLOGY | 2010年 / 185卷 / 01期

基金：

美国国家卫生研究院;

关键词：

NATURAL-KILLER-CELLS; RETINOIC-ACID; IN-VIVO; CUTTING EDGE; ACTIVATION RECEPTOR; MEDIATED REJECTION; DOWN-REGULATION; INFECTED-CELLS; TUMOR-CELLS; BONE-MARROW;

D O I：

10.4049/jimmunol.1000397

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Human tumors frequently express membrane-bound or soluble NK group 2, member D (NKG2D) ligands. This results in chronic engagement of NKG2D on the surfaces of NK and CD8(+) T cells and rapid internalization of the receptor. Although it is well appreciated that this phenomenon impairs NKG2D-dependent function, careful analysis of NKG2D-independent functions in cells chronically stimulated through NKG2D is lacking. Using a mouse model of chronic NKG2D ligand expression, we show that constant exposure to NKG2D ligands does not functionally impair NK cells and CD8(+) T cells in the context of viral infection. The Journal of Immunology, 2010, 185: 157-165.

引用

页码：157 / 165

页数：9

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