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© The Rockefeller University Press, 0022-1007/1997/12/1957/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 12, December 15, 1997 1957-1963

Article

Association with FcR{gamma} Is Essential for Activation Signal through NKR-P1 (CD161) in Natural Killer (NK) Cells and NK1.1+ T Cells

Noriko Arase*, Hisashi Arase*, Seung Yong Park*, Hiroshi Ohno*, Chisei Ra{ddagger}, and Takashi Saito*

From the * Division of Molecular Genetics, Center for Biological Science, Chiba University School of Medicine, Chiba 260, Japan; and the {ddagger} Department of Immunology, Juntendo University School of Medicine, Tokyo 113, Japan

Natural killer (NK) cells exhibit cytotoxicity against variety of tumor cells and virus-infected cells without prior sensitization and represent unique lymphocytes involved in primary host defense. NKR-P1 is thought to be one of NK receptors mediating activation signals because cross-linking of NKR-P1 activates NK cells to exhibit cytotoxicity and IFN-{gamma} production. However, molecular mechanism of NK cell activation via NKR-P1 is not well elucidated. In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcR{gamma} chain which is an essential component of Fc receptors for IgG and IgE. The association between FcR{gamma} and NKR-P1 is independent of Fc receptor complexes. Furthermore, NK cells from FcR{gamma}-deficient mice did not show cytotoxicity or IFN-{gamma} production upon NKR-P1 cross-linking. Similarly, NK1.1+ T cells from FcR{gamma}-deficient mice did not produce IFN-{gamma} upon NKR-P1 crosslinking. These findings demonstrate that the FcR{gamma} chain plays an important role in activation of NK cells via the NKR-P1 molecule.

Address correspondence to Takashi Saito, Division of Molecular Genetics, Center for Biological Science, Chiba University School of Medicine, 1-8-1 Inohana, Chuou-ku, Chiba 260, Japan. Phone: 81 43 226-2197; FAX: 81 43 222-1791; E-mail: saito{at}med.m.chiba-u.ac.jp

The first two authors contributed equally to this work.

1 Abbreviations used in this paper: {gamma}–/–, FcR{gamma}-deficient; ITAM, immunoreceptor tyrosine-based activation motif; ITIM, immunoreceptor tyrosine-based inhibition motif; KIR, killer inhibitory receptors.


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