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Sci Rep. 2017 Aug 17;7(1):8661. doi: 10.1038/s41598-017-08866-2.

Human cytomegalovirus escapes immune recognition by NK cells through the downregulation of B7-H6 by the viral genes US18 and US20.

Author information

1
The Lautenberg Center for General and Tumor Immunology, Institute for Medical Research Israel-Canada (IMRIC), Faculty of Medicine, Hebrew University Hadassah Medical School, Jerusalem, 91120, Israel.
2
Department for Vaccinology/Immune Aging and Chronic Infection, HZI, 38124, Braunschweig, Germany.
3
Clinical Virology Unit, Hadassah Hebrew University Medical Center, Jerusalem, 91120, Israel.
4
Department of Life Sciences and Systems Biology, University of Turin, 10123, Turin, Italy.
5
Laboratory of Molecular Genetics and Immunology, The Rockefeller University, 1230 York Avenue, New York, NY, 10065, USA.
6
Institute for Virology, Medical School Hannover, 30625, Hannover, Germany.
7
The Lautenberg Center for General and Tumor Immunology, Institute for Medical Research Israel-Canada (IMRIC), Faculty of Medicine, Hebrew University Hadassah Medical School, Jerusalem, 91120, Israel. oferm@ekmd.huji.ac.il.

Abstract

Human cytomegalovirus (HCMV) is a major human pathogen, causing serious diseases in immunocompromised populations and congenially infected neonates. One of the main immune cells acting against the virus are Natural Killer (NK) cells. Killing by NK cells is mediated by a small family of activating receptors such as NKp30 that interact with the cellular ligand B7-H6. The outcome of B7-H6-NKp30 interaction was, so far, mainly studied with regard to NK recognition and killing of tumors. Here, we demonstrated that the expression of B7-H6 is upregulated following HCMV infection and that HCMV uses two of its genes: US18 and US20, to interfere with B7-H6 surface expression, in a mechanism involving endosomal degradation, in order to evade NK cell recognition.

PMID:
28819195
PMCID:
PMC5561058
DOI:
10.1038/s41598-017-08866-2
[Indexed for MEDLINE]
Free PMC Article

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