The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


The Journal of Immunology, 2007, 179: 781-785.
Copyright © 2007 by The American Association of Immunologists, Inc.

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thorén, F. B.
Right arrow Articles by Hellstrand, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thorén, F. B.
Right arrow Articles by Hellstrand, K.

The CD16/CD56bright Subset of NK Cells Is Resistant to Oxidant-Induced Cell Death1

Fredrik B. Thorén, Ana I. Romero, Svante Hermodsson and Kristoffer Hellstrand2

Department of Infectious Medicine, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden

Phagocyte-derived reactive oxygen species ("oxygen radicals") have been ascribed a suppressive role in immunoregulation by inducing dysfunction and apoptotic cell death in lymphocytes. Earlier studies show that human NK cells are exceptionally sensitive to oxygen radical-induced apoptosis and functional inhibition. Two subsets of human CD56+ NK cells have been identified: the highly cytotoxic CD56dim cells which constitute >90% of NK cells in peripheral blood, and the less cytotoxic but efficiently cytokine-producing CD56bright cells. In this study, we demonstrate that the CD56bright subset of NK cells, in contrast to CD56dim cells, remains viable and functionally intact after exposure to phagocyte-derived or exogenously added oxygen radicals. The resistance of CD56bright cells to oxidative stress was accompanied by a high capacity of neutralizing exogenous hydrogen peroxide, and by a high cell-surface expression of antioxidative thiols. Our results imply that CD56bright NK cells are endowed with an efficient antioxidative defense system that protects them from oxygen radical-induced inactivation.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 This work was supported by Swedish Cancer Society, Swedish Research Council, Inga-Britt and Arne Lundberg Research Foundation, and Sahlgrenska Academy at Göteborg University.

2 Address correspondence and reprint requests to Dr. Kristoffer Hellstrand, Department of Infectious Medicine, Sahlgrenska Academy at Göteborg University, Guldhedsgatan 10b, S-413 46 Göteborg, Sweden. E-mail address: kristoffer.hellstrand{at}microbio.gu.se

3 Abbreviations used in this paper: PMN, polymorphonuclear phagocyte; MP, mononuclear phagocyte; MFI, median fluorescence intensity; ALM-633, Alexa-633 C5-maleimide; PARP, poly(ADP-ribose)polymerase; AIF, apoptosis-inducing factor.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2007 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2007 by The American Association of Immunologists, Inc. All rights reserved.