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

David B. Rosen, Jayaram Bettadapura, Mohammed Alsharifi, Porunelloor A. Mathew, Hilary S. Warren, Lewis L. Lanier

Research output: Contribution to journalArticle

181 Scopus citations

Abstract

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 NFA T-GFP reporter cells expressing CD3ζ NKR-P1A chimeric receptor; reciprocally, reporter cells with a CD3ζ-LLT1 chimeric receptor are stimulated by NKR-P1A. Moreover, LLT1 on target cells can inhibit NK cytotoxicity via interactions with NKR-P1A.

Original languageEnglish
Pages (from-to)7796-7799
Number of pages4
JournalJournal of Immunology
Volume175
Issue number12
DOIs
StatePublished - 15 Dec 2005

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