The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 7 November 2005. doi:10.1084/jem.20051044
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 9, 1289-1300
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 3553K)
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 Hwang, E. S.
Right arrow Articles by Glimcher, L. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hwang, E. S.
Right arrow Articles by Glimcher, L. H.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*L-SERINE
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

 IL-2 production in developing Th1 cells is regulated by heterodimerization of RelA and T-bet and requires T-bet serine residue 508

Eun Sook Hwang1,2, Jeong-Ho Hong4, and Laurie H. Glimcher2,3

1 Division of Molecular Life Sciences and College of Pharmacy, Ewha Womans University, Seoul, Korea 121-742
2 Department of Immunology and Infectious Diseases, Harvard School of Public Health
3 Department of Medicine, Harvard Medical School, Boston, MA 02115
4 Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139

CORRESPONDENCE Laurie H. Glimcher: lglimche{at}hsph.harvard.edu OR Eun Sook Hwang: eshwang{at}ewha.ac.kr

Interleukin (IL)-2 is the predominant cytokine that is produced by naive Th cells in a primary response. It is required for proliferation and differentiation of Th precursor cells into effector cells. Initial high-level IL-2 production is followed by its decline, and the concomitant induction of cytokines that are typical of the differentiated state. Although the factors that are responsible for the early induction of IL-2 are well defined, the mechanisms that are responsible for its down-regulation in later stages of Th development have not been studied as much. Previous work from our laboratory revealed a repressor function for the T-box transcription factor, T-bet, in IL-2 gene transcription. Here, we report that T-betS508 is required for the optimal repression of IL-2 production in developing Th1 cells. Phosphorylation of T-betS508 by casein kinase I and glycogen synthase kinase-3 kinases accompanies T-bet's interaction with the RelA nuclear factor–{kappa}B transcription factor. Heterodimerization of T-bet and RelA interferes with the binding of RelA to the IL-2 promoter, and hence, transcriptional activation of the IL-2 gene by RelA.

Abbreviations used: ChIP, chromatin immunoprecipitation; CKI, casein kinase 1; CREB, cyclic AMP response element binding protein; CREM, cyclic AMP resonsive element modulator gene; GSK, glycogen synthase kinase; MS, mass spectrometry; PKA, protein kinase A; S508, serine 508; Thp, Th precursor.


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