The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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Published online 10 July 2006 doi:10.1084/jem.20060514
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 8, 1843-1850
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BRIEF DEFINITIVE REPORT

 The herpesviral Fc receptor fcr-1 down-regulates the NKG2D ligands MULT-1 and H60

Tihana Lenac1, Matthias Budt2, Jurica Arapovic1, Milena Hasan1, Albert Zimmermann2, Hrvoje Simic1, Astrid Krmpotic1, Martin Messerle3, Zsolt Ruzsics4, Ulrich H. Koszinowski4, Hartmut Hengel2, and Stipan Jonjic1

1 Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia
2 Institute for Virology, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany
3 Institute for Virology, Hannover Medical School, 30625 Hannover, Germany
4 Max von Pettenkofer Institute, Ludwig Maximilians University of Munich, 80336 Munich, Germany

CORRESPONDENCE Stipan Jonjic: jstipan{at}medri.hr OR Hartmut Hengel Hartmut.Hengel{at}uni-duesseldorf.de

Members of the {alpha}- and ß-subfamily of herpesviridae encode glycoproteins that specifically bind to the Fc part of immunoglobulin (Ig)G. Plasma membrane resident herpesviral Fc receptors seem to prevent virus-specific IgG from activating antibody-dependent effector functions. We show that the mouse cytomegalovirus (MCMV) molecule fcr-1 promotes a rapid down-regulation of NKG2D ligands murine UL16-binding protein like transcript (MULT)-1 and H60 from the cell surface. Deletion of the m138/fcr-1 gene from the MCMV genome attenuates viral replication to natural killer (NK) cell response in an NKG2D-dependent manner in vivo. A distinct N-terminal module within the fcr-1 ectodomain in conjunction with the fcr-1 transmembrane domain was required to dispose MULT-1 to degradation in lysosomes. In contrast, down-modulation of H60 required the complete fcr-1 ectodomain, implying independent modes of fcr-1 interaction with the NKG2D ligands. The results establish a novel viral strategy for down-modulating NK cell responses and highlight the impressive diversity of Fc receptor functions.

T. Lenac and M. Budt contributed equally to this work.


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