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Th17 cells: effector T cells with inflammatory properties Korn T; Oukka M; Kuchroo V; Bettelli ESemin Immunol 2007[Dec]; 19 (6): 362-71Upon activation, naive CD4(+) T cells differentiate into effector T cells with specific effector functions and cytokine profiles. The Th1/Th2 paradigm has recently been reevaluated to include a third population of T helper cells, producing IL-17 and designated Th17. The differentiation of Th17 cells requires the coordinate and specific action of the proinflammatory cytokine IL-6 and the immunosuppressive cytokine TGF-beta. In addition, the IL-12 family member IL-23 is involved in the maintenance of these cells. Analogous to other T helper cell subsets, Th17 commitment is initiated by sequential involvement of STAT molecules, i.e. STAT3 downstream of cytokine receptors, and specific transcription factors, i.e. ROR-gammat. Recent data also support the existence of a complex network of cytokines regulating Th17 cells. Clearly, the specific effector functions of Th17 cells expand beyond previously described effects of Th1 and Th2 immunity, with specific roles in host defense against certain pathogens and in organ-specific autoimmunity. The potential dynamics of Th17 cell populations and their interplay with other inflammatory cells in the induction of tissue inflammation in host defense and organ-specific autoimmunity are discussed.|*Autoimmunity[MESH]|Animals[MESH]|Cell Differentiation[MESH]|Cytokines/immunology/*metabolism[MESH]|Humans[MESH]|Immunity, Innate[MESH]|Inflammation/*immunology[MESH]|Interleukin-17/*immunology[MESH]|STAT3 Transcription Factor/metabolism[MESH]|T-Lymphocyte Subsets/immunology/metabolism[MESH]|T-Lymphocytes, Helper-Inducer/*immunology/metabolism[MESH]|Transcription Factors/metabolism[MESH]|Transforming Growth Factor beta/metabolism[MESH] |
