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Transcriptional regulation of Th17 cell differentiation Ivanov II; Zhou L; Littman DRSemin Immunol 2007[Dec]; 19 (6): 409-17The paradigm of effector T helper cell differentiation into either Th1 or Th2 lineages has been profoundly shaken by the discovery of T cells that secrete IL-17 and other inflammatory cytokines. This subset, referred to as Th17, is centrally involved in autoimmune disease and is important in host defense at mucosal surfaces. In mouse, a series of cytokines, including IL-6, IL-21, IL-23, and TGF-beta, function sequentially or synergistically to induce the Th17 lineage. Other cytokines, including IL-2, IL-4, IFNgamma, and IL-27, inhibit differentiation of this lineage. Here we review how the nuclear orphan receptor RORgammat functions to coordinate the diverse cytokine-induced signals and thus controls Th17 cell differentiation.|Animals[MESH]|Cell Differentiation[MESH]|Cytokines/immunology/*metabolism[MESH]|Forkhead Transcription Factors/*metabolism[MESH]|Humans[MESH]|Interferon Regulatory Factors/*metabolism[MESH]|Interleukin-17/immunology/*metabolism[MESH]|Nuclear Receptor Subfamily 1, Group F, Member 3[MESH]|Receptors, Retinoic Acid/*metabolism[MESH]|Receptors, Thyroid Hormone/*metabolism[MESH]|T-Lymphocyte Subsets/cytology/immunology/metabolism[MESH]|T-Lymphocytes, Helper-Inducer/cytology/immunology/*metabolism[MESH]|Transcription, Genetic[MESH] |
