The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online
doi:10.1084/jem.20072254
The Journal of Experimental Medicine, Vol. 205, No. 10, 2349-2357
The Rockefeller University Press, 0022-1007 $30.00
© Gilchrist et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 3892K)
Right arrow PPT slides of all figures
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 Gilchrist, M.
Right arrow Articles by Aderem, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gilchrist, M.
Right arrow Articles by Aderem, A.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

ARTICLE

Activating transcription factor 3 is a negative regulator of allergic pulmonary inflammation

Mark Gilchrist1, William R. Henderson, Jr.2, April E. Clark1, Randi M. Simmons1, Xin Ye2, Kelly D. Smith3, and Alan Aderem1

1 Institute for Systems Biology, Seattle, WA 98103
2 Center for Allergy and Inflammation, Department of Medicine and 3 Department of Pathology, University of Washington, Seattle, WA 98109

CORRESPONDENCE Alan Aderem: aderem{at}systemsbiology.org

We recently demonstrated the pivotal role of the transcription factor (TF) activating TF 3 (ATF3) in dampening inflammation. We demonstrate that ATF3 also ameliorates allergen-induced airway inflammation and hyperresponsiveness in a mouse model of human asthma. ATF3 expression was increased in the lungs of mice challenged with ovalbumin allergen, and this was associated with its recruitment to the promoters of genes encoding Th2-associated cytokines. ATF3-deficient mice developed significantly increased airway hyperresponsiveness, pulmonary eosinophilia, and enhanced chemokine and Th2 cytokine responses in lung tissue and in lung-derived CD4+ lymphocytes. Although several TFs have been associated with enhanced inflammatory responses in the lung, ATF3 attenuates the inflammatory responses associated with allergic airway disease.


Abbreviations used: ATF3, activating TF 3; BAL, bronchoalveolar lavage; ChIP, chromatin immunoprecipitation; OVA, ovalbumin; TF, transcription factor; TSS, transcription start site.

M. Gilchrist and W.R. Henderson Jr. contributed equally to this paper.

© 2008 Gilchrist et al. 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/).


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 Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



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