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The Journal of Immunology, 2005, 175: 7796-7799.
Copyright © 2005 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Lectin-Like Transcript-1 Is a Ligand for the Inhibitory Human NKR-P1A Receptor1

David B. Rosen*, Jayaram Bettadapura{dagger}, Mohammed Alsharifi{dagger}, Porunelloor A. Mathew{ddagger}, Hilary S. Warren2,{dagger} and Lewis L. Lanier2,3,*

* Department of Microbiology and Immunology, The Cancer Research Institute, and Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143; {dagger} Division of Immunology and Genetics, The John Curtin School of Medical Research, The Australian National University, Canberra City, Australian Capital Territory, Australia; and {ddagger} 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{zeta}-NKR-P1A chimeric receptor; reciprocally, reporter cells with a CD3{zeta}-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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