Cutting edge: Lectin-like transcript-1 is a ligand for the inhibitory human NKR-P1A receptor

被引：215

作者：

Rosen, DB

Bettadapura, Y

Alsharifi, M

Mathew, PA

Warren, HS

Lanier, LL

机构：

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

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

[3] Australian Natl Univ, John Curtin Sch Med Res, Div Immunol & Genet, Canberra, ACT, Australia

[4] Univ N Texas, Hlth Sci Ctr, Dept Mol Biol & Immunol, Ft Worth, TX 76107 USA

[5] Univ N Texas, Hlth Sci Ctr, Inst Canc Res, Ft Worth, TX 76107 USA

来源：

JOURNAL OF IMMUNOLOGY | 2005年 / 175卷 / 12期

关键词：

D O I：

10.4049/jimmunol.175.12.7796

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Increasingly, roles are emerging for C-type lectin receptors in immune regulation. One receptor whose function has remained largely enigmatic is human NYR-P1A (CD161), present on NK cells and subsets of T cells. In this study, we demonstrate that the lectin-like transcript-1 (LLT1) is a physiologic ligand for NKR-P1A. LLT1-conposomes bind to NKR-P1A(+) cells, and binding taining is inhibited by anti-NYR-P1A mAb. Additionally, LLT1 activates NFAT-GFP reporter cells expressing a CD3 xi-NYR-P1A chimeric receptor; reciprocally, reporter cells with a CD3-LLT1 chimeric receptor are stimulated by NKR-P1A. Moreover, LLT1 on target cells can inhibit NK cytotoxicity via interactions with NYR-P1A.

引用

收藏

页码：7796 / 7799

页数：4

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