The Journal of Experimental Medicine
ELISpot, FluoroSpot and ELISA kits from Mabtech
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 274K)
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 Cauley, L. S.
Right arrow Articles by Swain, S. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cauley, L. S.
Right arrow Articles by Swain, S. L.
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, 0022-1007/1997/7/71/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 1, July 7, 1997 71-81

Articles

Transferable Anergy: Superantigen Treatment Induces CD4+ T Cell Tolerance That Is Reversible and Requires CD4–CD8– Cells and Interferon {gamma}

Linda S. Cauley*, Keith A. Cauley*, Fillipa Shub{ddagger}, Gail Huston*, and Susan L. Swain*

From the * Trudeau Institute, Saranac Lake, New York 12983; and {ddagger} Cancer Center, University of California at San Diego, La Jolla, California 92093

Bacterial superantigens induce peripheral unresponsiveness in CD4+ T cell populations that express appropriate Vβ chains. We have used Vβ3/V{alpha}11 T cell receptor transgenic (Tg) mice and the Vβ3-specific superantigen staphylococcal enterotoxin A (SEA) to further investigate the mechanisms that contribute to such unresponsiveness. As in other models, in vivo exposure to SEA rendered the Tg CD4+ cells unresponsive to subsequent restimulation in vitro with antigen or mitogens. However, when the SEA-treated CD4+ cells were completely purified away from all other contaminating cells, they regained the ability to proliferate and secrete cytokines. Moreover, enriched CD4–CD8– cells from the SEA-treated mice suppressed the responses of fresh control CD4+ cells in mixed cultures indicating that the apparent "anergy" was both transferable and reversible. Further analysis demonstrated that interferon {gamma}, but not the Fas receptor, played a critical role in the suppression.

Address correspondence to Dr. Susan L. Swain, Director, Trudeau Institute, P.O. Box 59, 100 Algonquin Ave., Saranac Lake, NY 12983. Phone: 518-891-3080; FAX: 518-891-5126; E-mail: sswain{at}northnet.org. The present address of K.A. Cauley is the Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405.

1Abbreviations used in this paper: AICD, activation-induced cell death; C', complement; DN, CD4–CD8– double negative; F/S, forward and side light scatter; mRNA, messenger RNA; PCCF, peptide fragment of pigeon cytochrome; PI, propidium iodide; RT, reverse transcriptase; SAg, superantigen; SEA, staphylococcal enterotoxin A; TdR, [H3]thymidine; TdT, terminal deoxynucleotidyl transferase; Tg, transgenic.


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