Nature Immunology
6, 515 - 523 (2005)
Published online: 10 April 2005; | doi:10.1038/ni1190
Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirusTal I Arnon1, Hagit Achdout1, Ofer Levi1, Gal Markel1, Nivin Saleh2, Gil Katz1, Roi Gazit1, Tsufit Gonen-Gross1, Jacob Hanna1, Efrat Nahari3, Angel Porgador4, Alik Honigman5, Bodo Plachter6, Dror Mevorach3, Dana G Wolf2, 7
& Ofer Mandelboim1, 71
The Lautenberg Center for General and Tumor Immunology, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel. 2
Clinical Virology Unit, Department of Clinical Microbiology and Infectious Diseases, Hadassah Medical Center, Jerusalem 91120, Israel. 3
Laboratory for Cellular and Molecular Immunology, Rheumatology Unit, Department of Medicine, Hadassah-Hebrew University, POB 12000, Kiryat Hadassah, Jerusalem 91120, Israel. 4
Department of Microbiology and Immunology, Faculty of Health Sciences and the Cancer Research Center Ben-Gurion University of the Negev, Beer Sheva 84105, Israel. 5
Virology Department, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel. 6
Institute for Virology, Johannes Gutenberg University of Mainz, 55101 Mainz, Germany. 7
These authors contributed equally to this work.
Correspondence should be addressed to Ofer Mandelboim oferman@md2.huji.ac.ilHuman cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3 from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor.
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