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Int Immunol. 2009 May;21(5):489-98. doi: 10.1093/intimm/dxp021. Epub 2009 Mar 4.

Th17 cells: from precursors to players in inflammation and infection.

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1
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Louis Pasteur Avenue, HIM 780, Boston, MA 02115, USA.

Abstract

Upon activation, naive CD4(+) T cells differentiate into different lineages of effector T(h) subsets. Each subset is characterized by its unique cytokine profile and biological functions. T(h)17, a newly described T(h) 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 T(h)17 subset. Transforming growth factor beta (TGF) together with IL-6 or IL-21 initiates the differentiation while IL-23 stabilizes the generation of T(h)17 cells. The transcription factors of T(h)17 cells [retinoid-related orphan receptor (ROR) gammat, ROR-alpha and signal transducer and activator of transcription-3] have been described recently. Since TGF-beta is essential for the generation of both T(h)17 and regulatory T (T(reg)) cells from naive T cells, which suggests a developmental link between T(h)17 and T(reg) cells. Functions of these two subsets of T cells are, however, opposite to each other; T(h)17 cells are highly pathogenic during the inflammatory process while T(reg) cells are crucial for inhibiting tissue inflammation and maintaining self-tolerance. Here, we review the recent information on differentiation and effector functions of T(h)17 cells during inflammatory conditions.

PMID:
19261692
PMCID:
PMC2675030
DOI:
10.1093/intimm/dxp021
[Indexed for MEDLINE]
Free PMC Article
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