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A correction to this article has been published: DeVoss et al., J. Exp. Med. 204 (1) 203
Published online 20 November 2006 doi:10.1084/jem.20061864
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 12, 2727-2735
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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.


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