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A correction to this article has been published: Cerwenka, J. Exp. Med. 206 (3) 723
Published online
doi:10.1084/jem.20090225
The Journal of Experimental Medicine, Vol. 206, No. 2, 265-268
The Rockefeller University Press, 0022-1007 $30.00
© Cerwenka
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COMMENTARY

 New twist on the regulation of NKG2D ligand expression

Adelheid Cerwenka

A.C. is at Group of Innate Immunity, German Cancer Research Center, 69120 Heidelberg, Germany

CORRESPONDENCE A.C.: a.cerwenka{at}dkfz.de


ABSTRACT
The NK cell–activating receptor NKG2D plays a prominent role in antitumor immune responses. Expression of the multiple NKG2D ligands must be tightly controlled to guarantee that NK cells attack tumors but not healthy cells. New data reveal a novel mechanism of posttranslational regulation of the mouse NKG2D ligand MULT1, in which MULT1 is ubiquitinated and degraded in healthy cells. In response to UV stress or heat shock, ubiquitination of MULT1 decreases and cell surface expression increases. Thus, targeting the ubiquitination machinery in cancer cells might increase the susceptibility of tumors to NK cell–mediated killing.

© 2009 Cerwenka
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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Related Article

Posttranslational regulation of the NKG2D ligand Mult1 in response to cell stress
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