The Journal of Experimental Medicine
Keystone Symposia
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online July 23, 2007
doi:10.1084/jem.20062456
The Journal of Experimental Medicine, Vol. 204, No. 8, 1749-1755
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Naoe et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 Naoe, Y.
Right arrow Articles by Taniuchi, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Naoe, Y.
Right arrow Articles by Taniuchi, I.
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

 Repression of interleukin-4 in T helper type 1 cells by Runx/Cbfß binding to the Il4 silencer

Yoshinori Naoe1, Ruka Setoguchi1, Kaori Akiyama1,2, Sawako Muroi2, Masahiko Kuroda3, Farah Hatam4, Dan R. Littman4, and Ichiro Taniuchi1,2

1 Institute of Physical and Chemical Research, Research Center for Allergy and Immunology, Turumi-ku, Yokohama, Kanagawa 230-0045, Japan
2 Precursory Research for Embryonic Sciences and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan
3 Tokyo Medical University, Shinjuku-ku, Tokyo 160-8402, Japan
4 Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016

CORRESPONDENCE Ichiro Taniuchi:taniuchi{at}rcai.riken.jp

Interferon {gamma} (IFN{gamma}) is the hallmark cytokine produced by T helper type 1 (Th1) cells, whereas interleukin (IL)-4 is the hallmark cytokine produced by Th2 cells. Although previous studies have revealed the roles of cytokine signaling and of transcription factors during differentiation of Th1 or Th2 cells, it is unclear how the exclusive expression pattern of each hallmark cytokine is established. The DNaseI hypersensitivity site IV within the mouse Il4 locus plays an important role in the repression of Il4 expression in Th1 cells, and it has been named the Il4 silencer. Using Cbfß- or Runx3-deficient T cells, we show that loss of Runx complex function results in derepression of IL-4 in Th1 cells. Binding of Runx complexes to the Il4 silencer was detected in naive CD4+ T cells and Th1 cells, but not in Th2 cells. Furthermore, enforced expression of GATA-3 in Th1 cells inhibited binding of Runx complexes to the Il4 silencer. Interestingly, T cell–specific inactivation of the Cbfß gene in mice led to elevated serum immunoglobulin E and airway infiltration. These results demonstrate critical roles of Runx complexes in regulating immune responses, at least in part, through the repression of the Il4 gene.

Abbreviations used: ChIP, chromatin immunoprecipitation; CNS, conserved noncoding sequence; HS, hypersensitive.


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