The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 21 August 2000.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 212K)
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 CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tsytsykova, A. V.
Right arrow Articles by Goldfeld, A. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsytsykova, A. V.
Right arrow Articles by Goldfeld, A. E.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH
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?
© The Rockefeller University Press, 0022-1007/2000/8/581/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 4, August 21, 2000 581-586

Brief Definitive Report

Nuclear Factor of Activated T Cells Transcription Factor Nfatp Controls Superantigen-Induced Lethal Shock

Alla V. Tsytsykovaa and Anne E. Goldfelda

a From The Center for Blood Research and Harvard Medical School and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
The Center for Blood Research and Harvard Medical School, 800 Huntington Ave., Boston, MA 02115.617-278-3454617-278-3351

goldfeld{at}cbr.med.harvard.edu

Tumor necrosis factor {alpha} (TNF-{alpha}) is the key mediator of superantigen-induced T cell lethal shock. Here, we show that nuclear factor of activated T cells transcription factor, NFATp, controls susceptibility to superantigen-induced lethal shock in mice through its activation of TNF-{alpha} gene transcription. In NFATp-deficient mice, T cell stimulation leads to delayed induction and attenuation of TNF-{alpha} mRNA levels, decreased TNF-{alpha} serum levels, and resistance to superantigen-induced lethal shock. By contrast, after lipopolysaccharide (LPS) challenge, serum levels of TNF-{alpha} and susceptibility to shock are unaffected. These results demonstrate that NFATp is an essential activator of immediate early TNF-{alpha} gene expression in T cells and they present in vivo evidence of the inducer- and cell type–specific regulation of TNF-{alpha} gene expression. Furthermore, they suggest NFATp as a potential selective target in the treatment of superantigen-induced lethal shock.

Key Words: tumor necrosis factor {alpha} • staphylococcal enterotoxin B • lipopolysaccharide • transcription • toxic shock

© 2000 The Rockefeller University Press


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?




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