The Journal of Experimental Medicine
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Published 17 February 2004. doi:10.1084/jem.20031885
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 4, 525-533
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Activation of Natural Killer Cells and Dendritic Cells upon Recognition of a Novel CD99-like Ligand by Paired Immunoglobulin-like Type 2 Receptor

Ikuo Shiratori1,2, Kouetsu Ogasawara3, Takashi Saito1,4, Lewis L. Lanier3, and Hisashi Arase1,2

1 Department of Molecular Genetics, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan
2 Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan
3 Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, CA 94143
4 Laboratory of Cell Signaling, Institute of Physical and Chemical Research, Reseach Center for Allergy and Immunology, Yokohama 230-0045, Japan

Address correspondence to Hisashi Arase, Dept. of Molecular Genetics, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuoku, Chiba 260-8670, Japan. Phone: 81-43-226-2198; Fax: 81-43-222-1791; email: arase{at}faculty.chiba-u.jp

Paired receptors that consist of highly related activating and inhibitory receptors are widely involved in the regulation of the immune system. Here, we report a mouse orthologue of the human activating paired immunoglobulin-like type 2 receptor (PILR) ß, which was cloned from a cDNA library of natural killer (NK) cells based on its ability to associate with the DAP12 signaling adaptor protein. The activating PILRß was expressed not only on NK cells but also on dendritic cells and macrophages. Furthermore, we have identified a novel CD99-like molecule as a ligand for the activating PILRß and inhibitory PILR{alpha} receptors. Transcripts of PILR ligand are present in many tissues, including some T cell lines. Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRß. Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.

Key Words: natural killer cell receptor • tumor antigen • innate immunity • immunoglobulin superfamily • DAP12

T. Saito and L.L. Lanier contributed equally to this work.

The present address of H. Arase is the Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.

Abbreviations used in this paper: BM-DC, BM-derived DC; GFP, green fluorescent protein; IRES, internal ribosome entry site; ITAM, immunoreceptor tyrosine-based activation motif; ITIM, immunoreceptor tyrosine-based inhibitory motif; KIR, killer cell Ig-like receptor; MCMV, mouse cytomegalovirus; PILR, paired Ig-like type 2 receptor, PILR-L, PILR ligand.


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