Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Originally published in Science Express on 14 June 2007
Science 13 July 2007:
Vol. 317. no. 5835, pp. 256 - 260
DOI: 10.1126/science.1145697

Reports

Reciprocal TH17 and Regulatory T Cell Differentiation Mediated by Retinoic Acid

Daniel Mucida, Yunji Park, Gisen Kim, Olga Turovskaya, Iain Scott, Mitchell Kronenberg, Hilde Cheroutre*

The cytokine transforming growth factor–ß (TGF-ß) converts naïve T cells into regulatory T (Treg) cells that prevent autoimmunity. However, in the presence of interleukin-6 (IL-6), TGF-ß has also been found to promote the differentiation of naïve T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (TH17) cells, which promote autoimmunity and inflammation. This raises the question of how TGF-ß can generate such distinct outcomes. We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-ß–dependent immune responses, capable of inhibiting the IL-6–driven induction of proinflammatory TH17 cells and promoting anti-inflammatory Treg cell differentiation. These findings indicate that a common metabolite can regulate the balance between pro- and anti-inflammatory immunity.

La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.

* To whom correspondence should be addressed. E-mail: hilde{at}liai.org

Read the Full Text






ADVERTISEMENT
Click Me!

ADVERTISEMENT

To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)