A structural basis for the association of DAP12 with mouse, but not human, NKG2D

被引：113

作者：

Rosen, DB

Araki, M

Hamerman, JA

Chen, T

Yamamura, T

Lanier, LL

机构：

[1] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA

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

[3] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Immunol, Kodaira, Tokyo 187, Japan

来源：

JOURNAL OF IMMUNOLOGY | 2004年 / 173卷 / 04期

关键词：

D O I：

10.4049/jimmunol.173.4.2470

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Prior studies have revealed that alternative mRNA splicing of the mouse NKG2D gene generates receptors that associate with either the DAP10 or DAP12 transmembrane adapter signaling proteins. We report that NKG2D function is normal in human patients lacking functional DAP12, indicating that DAP10 is sufficient for human NKG2D signal transduction. Further, we show that human NKG2D is incapable of associating with DAP12 and provide evidence that structural differences in the transmembrane of mouse and human NKG2D account for the species-specific difference for this immune receptor.

引用

收藏

页码：2470 / 2478

页数：9

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