Natural killer (NK) cells have been implicated in early immune responses against certain viruses, including cytomegalovirus (CMV). CMV causes downregulation of class I major histocompatibility complex (MHC) expression in infected cells; however, it has been proposed that a class I MHC homolog encoded by CMV, UL18, may act as a surrogate ligand to prevent NK cell lysis of CMV-infected cells. In this study, we examined the role of UL18 in NK cell recognition and lysis using fibroblasts infected with either wild-type or UL18 knockout CMV virus, and by using cell lines transfected with the UL18 gene. In both systems, the expression of UL18 resulted in the enhanced killing of target cells. We also show that the enhanced killing is due to both UL18-dependent and -independent mechanisms, and that the killer cell inhibitory receptors (KIRs) and CD94/NKG2A inhibitory receptors for MHC class I do not play a role in affecting susceptibility of CMV-infected fibroblasts to NK cell–mediated cytotoxicity.
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18 May 1998
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May 18 1998
Modulation of Natural Killer Cell Cytotoxicity in Human Cytomegalovirus Infection: The Role of Endogenous Class I Major Histocompatibility Complex and a Viral Class I Homolog
Clement C. Leong,
Clement C. Leong
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Tara L. Chapman,
Tara L. Chapman
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Pamela J. Bjorkman,
Pamela J. Bjorkman
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Danuska Formankova,
Danuska Formankova
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Edward S. Mocarski,
Edward S. Mocarski
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Joseph H. Phillips,
Joseph H. Phillips
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Lewis L. Lanier
Lewis L. Lanier
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
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Clement C. Leong
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Tara L. Chapman
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Pamela J. Bjorkman
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Danuska Formankova
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Edward S. Mocarski
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Joseph H. Phillips
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Lewis L. Lanier
From the *Department of Immunobiology, DNAX Institute of Molecular and Cell Biology, Palo Alto, California 94304; the ‡Division of Biology 156-29 and Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125; and the §Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Address correspondence to Clement Leong, DNAX Research Institute, 901 California Ave., Palo Alto, CA 94304. Phone: 650-496-1241; Fax: 650-496-1200; E-mail: [email protected]
DNAX Research Institute is supported by the Schering Plough Corporation. T.L Chapman is supported by a National Defense Science and Engineering Pre-Doctoral Fellowship.
Received:
December 03 1997
Revision Received:
February 26 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1998
J Exp Med (1998) 187 (10): 1681–1687.
Article history
Received:
December 03 1997
Revision Received:
February 26 1998
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Clement C. Leong, Tara L. Chapman, Pamela J. Bjorkman, Danuska Formankova, Edward S. Mocarski, Joseph H. Phillips, Lewis L. Lanier; Modulation of Natural Killer Cell Cytotoxicity in Human Cytomegalovirus Infection: The Role of Endogenous Class I Major Histocompatibility Complex and a Viral Class I Homolog . J Exp Med 18 May 1998; 187 (10): 1681–1687. doi: https://doi.org/10.1084/jem.187.10.1681
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