The Journal of Experimental Medicine
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Published online 10 January 2005 doi:10.1084/jem.20041617
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 2, 211-220
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ARTICLE

 NK cell activation through the NKG2D ligand MULT-1 is selectively prevented by the glycoprotein encoded by mouse cytomegalovirus gene m145

Astrid Krmpotic1, Milena Hasan1, Andrea Loewendorf2, Tanja Saulig1, Anne Halenius3, Tihana Lenac1, Bojan Polic1, Ivan Bubic1, Anja Kriegeskorte4, Ester Pernjak-Pugel1, Martin Messerle2, Hartmut Hengel3, Dirk H. Busch4, Ulrich H. Koszinowski5, and Stipan Jonjic1

1 Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia
2 Virus Cell Interaction Group, ZAMED, Medical Faculty, Martin Luther University of Halle-Wittenberg, 06120 Halle, Germany
3 Robert Koch-Institute, Division of Viral Infections, 13353 Berlin, Germany
4 Institute for Medical Microbiology, Immunology and Hygiene, Technical University Munich, 80336 Munich, Germany
5 Max von Pettenkofer Institute, Ludwig Maximilians University of Munich, 80336 Munich, Germany

CORRESPONDENCE Stipan Jonjic: jstipan{at}medri.hr

The NK cell–activating receptor NKG2D interacts with three different cellular ligands, all of which are regulated by mouse cytomegalovirus (MCMV). We set out to define the viral gene product regulating murine UL16-binding protein-like transcript (MULT)-1, a newly described NKG2D ligand. We show that MCMV infection strongly induces MULT-1 gene expression, but surface expression of this glycoprotein is nevertheless completely abolished by the virus. Screening a panel of MCMV deletion mutants defined the gene m145 as the viral regulator of MULT-1. The MCMV m145-encoded glycoprotein turned out to be necessary and sufficient to regulate MULT-1 by preventing plasma membrane residence of MULT-1. The importance of MULT-1 in NK cell regulation in vivo was confirmed by the attenuating effect of the m145 deletion that was lifted after NK cell depletion. Our findings underline the significance of escaping MULT-1/NKG2D signaling for viral survival and maintenance.

Abbreviations used: HCMV, human CMV; MCMV, mouse CMV; MEF, mouse embryonic fibroblast; MOI, multiplicity of infection; MULT, murine UL16-binding protein-like transcript; ORF, open reading frame; RAE, retinoic acid early inducible.

H. Hengel's present address is Institute for Virology, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.

The online version of this article contains supplemental material.


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