Abstract:
:Mutations in the gene encoding the transcription factor autoimmune regulator (AIRE) are responsible for autoimmune polyendocrinopathy candidiasis ectodermal dystrophy syndrome. AIRE directs expression of tissue-restricted antigens in the thymic medulla and in lymph node stromal cells and thereby substantially contributes to induction of immunological tolerance to self-antigens. Data from experimental mouse models showed that AIRE deficiency leads to impaired deletion of autospecific T-cell precursors. However, a potential role for AIRE in the function of regulatory T-cell populations, which are known to play a central role in prevention of immunopathology, has remained elusive. Regulatory T cells of CD8(+)CD28(low) phenotype efficiently control immune responses in experimental autoimmune and colitis models in mice. Here we show that CD8(+)CD28(low) regulatory T lymphocytes from AIRE-deficient mice are transcriptionally and phenotypically normal and exert efficient suppression of in vitro immune responses, but completely fail to prevent experimental colitis in vivo. Our data therefore demonstrate that AIRE plays an important role in the in vivo function of a naturally occurring regulatory T-cell population.
journal_name
Proc Natl Acad Sci U S Aauthors
Pomié C,Vicente R,Vuddamalay Y,Lundgren BA,van der Hoek M,Enault G,Kagan J,Fazilleau N,Scott HS,Romagnoli P,van Meerwijk JPdoi
10.1073/pnas.1107136108subject
Has Abstractpub_date
2011-07-26 00:00:00pages
12437-42issue
30eissn
0027-8424issn
1091-6490pii
1107136108journal_volume
108pub_type
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