A selective role of NKG2D in inflammatory and autoimmune diseases

被引：39

作者：

Guerra, Nadia ^{[1
,2
,3
]}

Pestal, Kathleen ^{[1
,2
]}

Juarez, Tiffany ^{[1
,2
]}

Beck, Jennifer ^{[1
,2
]}

Tkach, Karen ^{[1
,2
]}

Wang, Lin ^{[1
,2
]}

Raulet, David H. ^{[1
,2
]}

机构：

[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

[2] Univ Calif Berkeley, Canc Res Lab, Berkeley, CA 94720 USA

[3] Univ London Imperial Coll Sci Technol & Med, Dept Life Sci, London SW7 2AZ, England

来源：

CLINICAL IMMUNOLOGY | 2013年 / 149卷 / 03期

基金：

美国国家卫生研究院;

关键词：

NKG2D; NK cells; EAE; NOD; Type; 1; diabetes; Intestinal inflammation; NATURAL-KILLER-CELLS; T-CELLS; MIC LIGANDS; NK CELLS; BLOCKADE; EXPRESSION; INNATE; INJURY; ENCEPHALOMYELITIS; IMMUNORECEPTOR;

D O I：

10.1016/j.clim.2013.09.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The NKG2D activating receptor has been implicated in numerous autoimmune diseases. We tested the role of NKG2D in models of autoimmunity and inflammation using NKG2D knockout mice and antibody blockade experiments. The severity of experimental autoimmune encephalitis (EAE) was decreased in NKG2D-deficient mice when the disease was induced with a limiting antigen dose, but unchanged with an optimal antigen dose. Surprisingly, however, NKG2D deficiency had no detectable effect in several other models, including two models of type 1 diabetes, and a model of intestinal inflammation induced by poly(I:C). NKG2D antibody blockade in normal mice also failed to inhibit disease in the NOD diabetes model or the intestinal inflammation model. Published evidence using NKG2D knockout mice demonstrated a role for NKG2D in mouse models of atherosclerosis and liver inflammation, as well as in chronic obstructive pulmonary disease. Therefore, our results suggest that NKG2D plays selective roles in inflammatory diseases. (C) 2013 Elsevier Inc. All rights reserved.

引用

页码：432 / 439

页数：8

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