International Immunology Advance Access first published online on March 4, 2009
This version published online on March 5, 2009
International Immunology, doi:10.1093/intimm/dxp021
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review-article |
Th17 cells: from precursors to players in inflammation and infection
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Louis Pasteur Avenue, HIM 780, Boston, MA 02115, USA
Correspondence to: Correspondence to: V. K. Kuchroo; E-mail: vkuchroo{at}rics.bwh.harvard.edu
Upon activation, naive CD4+ T cells differentiate into different lineages of effector Th subsets. Each subset is characterized by its unique cytokine profile and biological functions. Th17, a newly described Th subset that produces IL-17, IL-17F and IL-22 in preference to other cytokines, has been shown to play an important role in clearing specific pathogens and in inducing autoimmune tissue inflammations. Over the last 2–3 years, significant progress has been made to understand the development and biological functions of Th17 subset. Transforming growth factor β (TGF) together with IL-6 or IL-21 initiates the differentiation while IL-23 stabilizes the generation of Th17 cells. The transcription factors of Th17 cells [retinoid-related orphan receptor (ROR) 
t, ROR-
and signal transducer and activator of transcription-3] have been described recently. Since TGF-β is essential for the generation of both Th17 and regulatory T (Treg) cells from naive T cells, which suggests a developmental link between Th17 and Treg cells. Functions of these two subsets of T cells are, however, opposite to each other; Th17 cells are highly pathogenic during the inflammatory process while Treg cells are crucial for inhibiting tissue inflammation and maintaining self-tolerance. Here, we review the recent information on differentiation and effector functions of Th17 cells during inflammatory conditions.
Keywords: autoimmunity, cytokines, infection, regulatory T cells, Th subsets
This paper was erroneously published as an Original article in error. The publisher wishes to point out that this paper is a Review article.
Received 6 February 2009, accepted 9 February 2009.
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