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

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.