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CUTTING EDGE |
* Department of Microbiology and Immunology, The Cancer Research Institute, and Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143;
Division of Immunology and Genetics, The John Curtin School of Medical Research, The Australian National University, Canberra City, Australian Capital Territory, Australia; and
Department of Molecular Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107
Increasingly, roles are emerging for C-type lectin receptors in immune regulation. One receptor whose function has remained largely enigmatic is human NKR-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-containing liposomes bind to NKR-P1A+ cells, and binding is inhibited by anti-NKR-P1A mAb. Additionally, LLT1 activates NFAT-GFP reporter cells expressing a CD3
-NKR-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 NKR-P1A.
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