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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1013-1020. Prepublished online as a Blood First Edition Paper on October 19, 2007; DOI 10.1182/blood-2007-06-096438. This Article Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2007-06-096438v1 111/3/1013    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Elias, K. M Articles by O'Shea, J. J Search for Related Content PubMed PubMed Citation Articles by Elias, K. M Articles by O'Shea, J. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 18, 2007 Accepted October 8, 2007 Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway Kevin M Elias, Arian Laurence*, Todd S Davidson, Geoffrey Stephens, Yuka Kanno, Ethan M Shevach, and John J O'Shea Howard Hughes Medical Institute National Institutes of Health Research Scholars Program, Bethesda, MD, United States Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, NIH/NIAMS, Bethesda, MD, United States Laboratory of Immunology, Cellular Immunology Section, NIH/ NIAID, Bethesda, MD, United States * Corresponding author; email: laurencea{at}mail.nih.gov. CD4+ helper T (Th) cells play a crucial role in the delicate balance between host defense and autoimmune disease. Two important populations of helper T cells are the proinflammatory, interleukin-17-producing (Th17) cells and the anti-inflammatory forkhead box P3 positive (FoxP3+) T regulatory (Treg) cells. Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RAR) inhibit the formation of Th17 cells and promote FoxP3 expression. Conversely, inhibition of retinoic acid signaling constrains transforming growth factor beta (TGF-1) induction of FoxP3. The effect of ATRA is mediated independent of interleukin 2, signal transducer and activator of transcription (Stat)5 and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. As previous studies have shown that vitamin A derivatives are protective in animal models of autoimmune disease, the current data suggest a previously unrecognized role for RAR in the regulation of CD4+ T cell differentiation and provide a mechanism for the anti-inflammatory effects of retinoic acid. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Muranski, A. Boni, P. A. Antony, L. Cassard, K. R. Irvine, A. Kaiser, C. M. Paulos, D. C. Palmer, C. E. Touloukian, K. Ptak, et al. Tumor-specific Th17-polarized cells eradicate large established melanoma Blood, July 15, 2008; 112(2): 362 - 373. [Abstract] [Full Text] [PDF]

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