The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 10 July 2006 doi:10.1084/jem.20060514
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 8, 1843-1850
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 2696K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lenac, T.
Right arrow Articles by Jonjic, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lenac, T.
Right arrow Articles by Jonjic, S.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*Protein
*UniGene
*Substance via MeSH
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

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.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS