Send to

Choose Destination
See comment in PubMed Commons below
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.

Author information

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


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.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Silverchair Information Systems Icon for PubMed Central
    Loading ...
    Support Center