Hdl Handle:
http://hdl.handle.net/10675.2/542
Title:
Spontaneous autoimmunity prevented by thymic expression of a single self-antigen
Authors:
DeVoss, Jason; Hou, Yafei; Johannes, Kellsey; Lu, Wen; Liou, Gregory I.; Rinn, John; Chang, Howard; Caspi, Rachel R. ( 0000-0002-7140-7671 ) ; Fong, Lawrence; Anderson, Mark S.
Abstract:
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.
Citation:
J Exp Med. 2006 Nov 27; 203(12):2727-2735
Issue Date:
27-Nov-2006
URI:
http://hdl.handle.net/10675.2/542
DOI:
10.1084/jem.20061864
PubMed ID:
17116738
PubMed Central ID:
PMC2118158
Type:
Article
ISSN:
1540-9538
Appears in Collections:
Department of Ophthalmology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorDeVoss, Jasonen_US
dc.contributor.authorHou, Yafeien_US
dc.contributor.authorJohannes, Kellseyen_US
dc.contributor.authorLu, Wenen_US
dc.contributor.authorLiou, Gregory I.en_US
dc.contributor.authorRinn, Johnen_US
dc.contributor.authorChang, Howarden_US
dc.contributor.authorCaspi, Rachel R.en_US
dc.contributor.authorFong, Lawrenceen_US
dc.contributor.authorAnderson, Mark S.en_US
dc.date.accessioned2012-10-26T16:26:35Z-
dc.date.available2012-10-26T16:26:35Z-
dc.date.issued2006-11-27en_US
dc.identifier.citationJ Exp Med. 2006 Nov 27; 203(12):2727-2735en_US
dc.identifier.issn1540-9538en_US
dc.identifier.pmid17116738en_US
dc.identifier.doi10.1084/jem.20061864en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/542-
dc.description.abstractThe 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.en_US
dc.rightsCopyright © 2006, The Rockefeller University Pressen_US
dc.subjectArticlesen_US
dc.titleSpontaneous autoimmunity prevented by thymic expression of a single self-antigenen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2118158en_US
dc.contributor.corporatenameDepartment of Ophthalmology-

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