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Originally published In Press as doi:10.1074/jbc.C600321200 on February 3, 2007

J. Biol. Chem., Vol. 282, Issue 13, 9358-9363, March 30, 2007
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STAT3 Regulates Cytokine-mediated Generation of Inflammatory Helper T Cells*

Xuexian O. Yang{ddagger}, Athanasia D. Panopoulos{ddagger}1, Roza Nurieva{ddagger}23, Seon Hee Chang{ddagger}3, Demin Wang§, Stephanie S. Watowich{ddagger}, and Chen Dong{ddagger}4

From the {ddagger}Department of Immunology, M.D. Anderson Cancer Center, Houston, Texas 77030 and the §Blood Research Institute, Blood Center of Wisconsin, Milwaukee, Wisconsin 53226

Interleukin-17 (IL-17)-producing helper T (TH) cells, named as THIL-17, TH17, or inflammatory TH (THi), have been recently identified as a novel effector lineage. However, how cytokine signals mediate THi differentiation is unclear. We found that IL-6 functioned to up-regulate IL-23R and that IL-23 synergized with IL-6 in promoting THi generation. STAT3, activated by both IL-6 and IL-23, plays a critical role in THi development. A hyperactive form of STAT3 promoted THi development, whereas this differentiation process was greatly impaired in STAT3-deficient T cells. Moreover, STAT3 regulated the expression of retinoic acid receptor-related orphan receptor {gamma}-T (ROR{gamma}t), a THi-specific transcriptional regulator; STAT3 deficiency impaired ROR{gamma}t expression and led to elevated expression of T-box expressed in T cells (T-bet) and Forkhead box P3 (Foxp3). Our data thus demonstrate a pathway whereby cytokines regulate THi differentiation through a selective STAT transcription factor that functions to regulate lineage-specific gene expression.

Received for publication, December 28, 2006 , and in revised form, January 16, 2007.

* This work was supported by research grants from the National Institutes of Health (to C. D. and D. W.), American Cancer Society (to D. W.), and M. D. Anderson Cancer Center (to S. S. W.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 Supported by an National Institutes of Health training grant and an American Legion Auxiliary Award.

2 Recipient of a scientist development grant from the American Heart Association.

3 Recipients of postdoctoral fellowships from the Arthritis Foundation.

4 A Cancer Research Institute Investigator and an M. D. Anderson Cancer Center Trust Fellow. To whom correspondence should be addressed. Fax: 713-563-0604; E-mail: cdong{at}mdanderson.org.


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