TY - JOUR
T1 - Cutting edge
T2 - Lectin-like transcript-1 is a ligand for the inhibitory human NKR-P1A receptor
AU - Rosen, David B.
AU - Bettadapura, Jayaram
AU - Alsharifi, Mohammed
AU - Mathew, Porunelloor A.
AU - Warren, Hilary S.
AU - Lanier, Lewis L.
PY - 2005/12/15
Y1 - 2005/12/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=29144444611&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.175.12.7796
DO - 10.4049/jimmunol.175.12.7796
M3 - Article
SN - 0022-1767
VL - 175
SP - 7796
EP - 7799
JO - Journal of Immunology
JF - Journal of Immunology
IS - 12
ER -