The Journal of Experimental Medicine
Accuri Cytometers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 20 November 2006 doi:10.1084/jem.20061864
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 12, 2727-2735
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Material Index
Right arrow Correction (v204,p203)
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 DeVoss, J.
Right arrow Articles by Anderson, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by DeVoss, J.
Right arrow Articles by Anderson, M. S.
Related Collections
Right arrowRelated Article
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?

ARTICLE

 Spontaneous autoimmunity prevented by thymic expression of a single self-antigen

Jason DeVoss1, Yafei Hou2, Kellsey Johannes1, Wen Lu1, Gregory I. Liou3, John Rinn4, Howard Chang4, Rachel R. Caspi5, Lawrence Fong2, and Mark S. Anderson1,2

1 Diabetes Center and 2 Department of Medicine, University of California, San Francisco, San Francisco, CA 94143
3 Department of Ophthalmology, Medical College of Georgia, Augusta, GA 30912
4 Cancer Biology Program, Stanford University School of Medicine, Stanford, CA 94305
5 Laboratory of Immunology, National Eye Institute, National Institutes of Health (NIH), Bethesda, MD 20892

CORRESPONDENCE Mark Anderson: manderson{at}diabetes.ucsf.edu

The expression of self-antigen in the thymus is believed to be responsible for the deletion of autoreactive T lymphocytes, a critical process in the maintenance of unresponsiveness to self. The Autoimmune regulator (Aire) gene, which is defective in the disorder autoimmune polyglandular syndrome type 1, has been shown to promote the thymic expression of self-antigens. A clear link, however, between specific thymic self-antigens and a single autoimmune phenotype in this model has been lacking. We show that autoimmune eye disease in aire-deficient mice develops as a result of loss of thymic expression of a single eye antigen, interphotoreceptor retinoid-binding protein (IRBP). In addition, lack of IRBP expression solely in the thymus, even in the presence of aire expression, is sufficient to trigger spontaneous eye-specific autoimmunity. These results suggest that failure of thymic expression of selective single self-antigens can be sufficient to cause organ-specific autoimmune disease, even in otherwise self-tolerant individuals.

Abbreviations used: Aire, autoimmune regulator; APECED, autoimmune polyendocrinopathy candidiasis ectodermal dystrophy; DKO, double knockout; EAU, experimental autoimmune uveitis; IRBP, interphotoreceptor retinoid-binding protein; mTEC, medullary thymic epithelial cell; PMF, peptide mass fingerprinting; S-Ag, retinal soluble antigen; TSA, tissue-specific self-antigen.


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?

Related Article

Me, myself, and eye
Ruth Williams
J. Exp. Med. 2006 203: 2566a. [Full Text] [PDF]



This article has been cited by other articles:



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