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Stockinger B, Veldhoen MDifferentiation and function of Th17 T cells. Curr Opin Immunol 19: 281-286

Division of Molecular Immunology, The MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London, UK. .
Current Opinion in Immunology (Impact Factor: 7.87). 07/2007; 19(3):281-6. DOI: 10.1016/j.coi.2007.04.005
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ABSTRACT IL-17-producing T cells have recently been classified as a new effector T-cell subset, termed Th17, which is distinct from Th1, Th2 and Treg subsets. There has been much progress in the past year, leading to identification of the molecular mechanisms that drive differentiation of Th17 T cells. This has helped to clarify many aspects of their role in host defense as well as in autoimmunity. Nevertheless, many intriguing questions remain to be answered regarding the regulation of Th17-mediated responses as well as their interactions with the other T-cell subsets. Furthermore, the role of pathogens and pathogen-derived molecules in influencing effector T-cell polarization needs to be re-evaluated in the light of the differentiation conditions that favor Th17 T-cell responses.

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    • "e l s e v i e r . c o m / l o c a t e / t o x i c o l variety of autoimmune diseases, including psoriasis and rheumatoid arthritis (Harrington et al., 2005; Park et al., 2005; Weaver et al., 2007; Stockinger and Veldhoen, 2007), the identification of ligands that regulate the RORs has been the focus of significant interest due to their potential for clinical use (Huh and Littman, 2012; Solt and Burris, 2012). Unlike most members of the nuclear receptor superfamily, RORs bind as monomers to ROR response element (RORE), consisting of an AGGTCA element preceded by an AT-rich sequence, in the promoter regulatory region of the target genes. "
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    • "IL-17 producing Th17 cells are represented in high numbers in the LP of the small intestine, where they play a role in protection against extracellular pathogens (103). The differentiation of Th17 cells is dependent on their expression of the transcription factor RORγt, and it is driven by signals from TGF-β and IL-21 or IL-6 (109). Additionally, Th17 cells require IL-23 for maturation and survival (110). "
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