Although activation of natural killer (NK) cytotoxicity is generally inhibited by target major histocompatibility complex (MHC) class I expression, subtle features of NK allorecognition suggest that NK cells possess receptors that are activated by target MHC I. The mouse Ly-49D receptor has been shown to activate NK cytotoxicity, although recognition of MHC class I has not been demonstrated previously. To define Ly-49D–ligand interactions, we transfected the mouse Ly-49D receptor into the rat NK line, RNK-16 (RNK.mLy-49D). As expected, anti– Ly-49D monoclonal antibody 12A8 specifically stimulated redirected lysis of the Fc receptor– bearing rat target YB2/0 by RNK.mLy-49D transfectants. RNK.mLy-49D effectors were tested against YB2/0 targets transfected with the mouse MHC I alleles H-2Dd, Db, Kk, or Kb. RNK.mLy-49D cells lysed YB2/0.Dd targets more efficiently than untransfected YB2/0 or YB2/0 transfected with Db, Kk, or Kb. This augmented lysis of H-2Dd targets was specifically inhibited by F(ab′)2 anti–Ly-49D (12A8) and F(ab′)2 anti–H-2Dd (34-5-8S). RNK.mLy-49D effectors were also able to specifically lyse Concanavalin A blasts isolated from H-2d mice (BALB/c, B10.D2, and DBA/2) but not from H-2b or H-2k mice. These experiments show that the activating receptor Ly-49D specifically interacts with the MHC I antigen, H-2Dd, demonstrating the existence of alloactivating receptors on murine NK cells.
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1 February 1999
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February 01 1999
Mouse Ly-49D Recognizes H-2Dd and Activates Natural Killer Cell Cytotoxicity
Mary C. Nakamura,
Mary C. Nakamura
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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Paul A. Linnemeyer,
Paul A. Linnemeyer
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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Eréne C. Niemi,
Eréne C. Niemi
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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Llewellyn H. Mason,
Llewellyn H. Mason
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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John R. Ortaldo,
John R. Ortaldo
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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James C. Ryan,
James C. Ryan
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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William E. Seaman
William E. Seaman
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
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Mary C. Nakamura,
Paul A. Linnemeyer,
Eréne C. Niemi,
Llewellyn H. Mason,
John R. Ortaldo,
James C. Ryan,
William E. Seaman
From the *Department of Medicine, University of California San Francisco, San Francisco, California 94143, and the Veterans Administration Medical Center, San Francisco, California 94121; the ‡Laboratory of Experimental Immunology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, Maryland 21702; and the §Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143
Address correspondence to Mary Nakamura, Immunology/Arthritis Section 111-R, Veterans Administration Medical Center, 4150 Clement St., San Francisco, CA 94121. Phone: 415-750-2104; Fax: 415-750-6920; E-mail: [email protected]
The first two authors contributed equally to this work.
Received:
June 29 1998
Revision Received:
October 09 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1999
J Exp Med (1999) 189 (3): 493–500.
Article history
Received:
June 29 1998
Revision Received:
October 09 1998
Citation
Mary C. Nakamura, Paul A. Linnemeyer, Eréne C. Niemi, Llewellyn H. Mason, John R. Ortaldo, James C. Ryan, William E. Seaman; Mouse Ly-49D Recognizes H-2Dd and Activates Natural Killer Cell Cytotoxicity . J Exp Med 1 February 1999; 189 (3): 493–500. doi: https://doi.org/10.1084/jem.189.3.493
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