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CUTTING EDGE |
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* Department of Microbiology and Immunology, Cancer Research Institute and Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143;
Department of Immunochemistry, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Solution Oriented Research for Science and Technology, Japan Science and Technology Agency, Saitama, Japan;
Division of Experimental Medicine, University of California, San Francisco, CA 94143; and
¶ Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital in Huddinge, Stockholm, Sweden
The killer cell Ig-like receptor (KIR) gene, KIR3DS1, has been implicated in slowing disease progression in HIV infection; however, little is known about its expression, function, or ligand specificity. Using retrovirally transduced NKL cells and peripheral blood NK cells from KIR3DS1-positive donors we assessed expression of this gene by flow cytometry and its function by in vitro assays measuring KIR3DS1-induced cell-mediated cytotoxicity and cytokine production. In the present study, we demonstrate that KIR3DS1 is expressed on peripheral blood NK cells and triggers both cytotoxicity and IFN-
production. Using cotransfection and coimmunoprecipitation, we found that KIR3DS1 associates with the ITAM-bearing adaptor, DAP12. Soluble KIR3DS1-Ig fusion proteins did not bind to EBV-transformed B lymphoid cell lines transfected with HLA-Bw4 80I or 80T allotypes, suggesting that if KIR3DS1 does recognize HLA-Bw4 ligands, this may be peptide dependent.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants AI64520 (to L.L.L.), AI52731 and AI41531 (to D.F.N.), AI06452 (to D.F.N. and L.L.L.), and by National Institute of Allergy and Infectious Diseases Grants K08-AI50779-03 and AI50779-04 (to W.H.C.). L.L.L. is an American Cancer Society Research Professor. J.M. was supported by a grant from the Åke Wiberg Foundation. D.B.R. was supported by a UCSF Chancellor’s Fellowship.
2 Address correspondence and reprint requests to Dr. William H. Carr, Department of Microbiology and Immunology, University of California, San Francisco, CA 94143; E-mail address: wcarr{at}partners.org or Dr. Lewis L. Lanier, Department of Microbiology and Immunology, University of California, Box 0414, 513 Parnassus Avenue, San Francisco, CA 94143; E-mail address: Lewis.Lanier{at}ucsf.edu
3 Abbreviations used in this paper: KIR, killer cell Ig-like receptor; IRES, internal ribosomal entry site; SSP, sequence specific primer.
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