TY - JOUR
T1 - The LLT1 receptor induces IFN-γ production by human natural killer cells
AU - Mathew, Porunelloor A.
AU - Chuang, Samuel S.
AU - Vaidya, Swapnil V.
AU - Kumaresan, Pappanaicken R.
AU - Boles, Kent S.
AU - Pham, Hoang Tuan K.
N1 - Funding Information:
The authors thank Dr. Wayne Lai (UT Southwestern Medical Center, Dallas, Texas) for his support and technical expertise in mAb production and Tejaswi Belavadi for technical assistance. Research supported in part by a grant, CA 85753 (to P.A.M.) from the National Institute of Health.
PY - 2004/3
Y1 - 2004/3
N2 - Natural killer cell functions are regulated by signals through activating and inhibitory receptors. These receptors belong to the immunoglobulin superfamily or the lectin superfamily. We have previously identified a lectin-like transcript, LLT1, expressed in human NK cells. In the present study, we have generated a monoclonal antibody, L9.7, that specifically binds LLT1 receptor and studied the functional role of LLT1 in human NK cells. Binding of mAb L9.7 to surface LLT1 induced IFN-γ production, but did not modulate cytotoxicity by YT cells, a human NK cell line. We further demonstrate that in resting NK cells as well as in IL-2 activated NK cells LLT1 induced IFN-γ production, but not cytotoxicity. Excess amounts of L9.7 mAb failed to increase natural or antibody-dependent cell-mediated cytolytic activity, whereas minimal amounts achieved maximal production of IFN-γ by YT and activated NK cells. These findings further support the separation of signaling pathways that regulate cytotoxicity and IFN-γ production in resting as well as activated NK cells.
AB - Natural killer cell functions are regulated by signals through activating and inhibitory receptors. These receptors belong to the immunoglobulin superfamily or the lectin superfamily. We have previously identified a lectin-like transcript, LLT1, expressed in human NK cells. In the present study, we have generated a monoclonal antibody, L9.7, that specifically binds LLT1 receptor and studied the functional role of LLT1 in human NK cells. Binding of mAb L9.7 to surface LLT1 induced IFN-γ production, but did not modulate cytotoxicity by YT cells, a human NK cell line. We further demonstrate that in resting NK cells as well as in IL-2 activated NK cells LLT1 induced IFN-γ production, but not cytotoxicity. Excess amounts of L9.7 mAb failed to increase natural or antibody-dependent cell-mediated cytolytic activity, whereas minimal amounts achieved maximal production of IFN-γ by YT and activated NK cells. These findings further support the separation of signaling pathways that regulate cytotoxicity and IFN-γ production in resting as well as activated NK cells.
KW - Human
KW - Immune regulation
KW - LLT1
KW - Natural killer cells
UR - http://www.scopus.com/inward/record.url?scp=1142285364&partnerID=8YFLogxK
U2 - 10.1016/j.molimm.2003.11.024
DO - 10.1016/j.molimm.2003.11.024
M3 - Article
C2 - 15104121
AN - SCOPUS:1142285364
VL - 40
SP - 1157
EP - 1163
JO - Molecular Immunology
JF - Molecular Immunology
SN - 0161-5890
IS - 16
ER -