Essential autocrine regulation by IL-21 in the generation of inflammatory T cells

Roza Nurieva (), Xuexian O. Yang, Gustavo Martinez, Yongliang Zhang, Athanasia D. Panopoulos, Li Ma, Kimberly Schluns, Qiang Tian, Stephanie S. Watowich, Anton M. Jetten and Chen Dong ()
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Roza Nurieva: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Xuexian O. Yang: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Gustavo Martinez: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Yongliang Zhang: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Athanasia D. Panopoulos: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Li Ma: Institute for Systems Biology, Seattle, Washington 98103, USA
Kimberly Schluns: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Qiang Tian: Institute for Systems Biology, Seattle, Washington 98103, USA
Stephanie S. Watowich: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Anton M. Jetten: Cell Biology Section, LRB, National Institutes of Health, NIEHS, Research Triangle Park, North Carolina 27709, USA
Chen Dong: M. D. Anderson Cancer Center, Houston, Texas 77030, USA

Nature, 2007, vol. 448, issue 7152, 480-483

Abstract: Interleukin (IL)-17 expressing helper T cells (TH17) have recently been identified as a effector subset involved in tissue inflammation. In this paper, it is shown that the cytokine IL-21 is induced downstream of IL-6 by a STAT3 dependent mechanism and participates in inducing TH17 cell differentiation in an autocrine and ROR-γ dependent manner

Date: 2007
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DOI: 10.1038/nature05969

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