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• W2079494090 abstract "Autoimmune inflammatory responses and the diseases that develop as a consequence are now thought to be driven through a novel non-Th(1) pathway. IL-23, together with additional factors including TGF-beta1 and IL-6, collectively generate and sustain a distinct CD4(+) 'Th(17) inflammation effector' T-cell subset characterized by its production of inflammatory chemokines and cytokines, including IL-17. With this paradigm shift in understanding of autoimmune inflammation pathogenesis comes exciting opportunities to identify and to target therapeutically molecules within the IL-23/Th(17) axis that are key to disease development." @default.
• W2079494090 created "2016-06-24" @default.
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• W2079494090 date "2006-12-01" @default.
• W2079494090 modified "2023-09-24" @default.
• W2079494090 title "The IL-23/Th17 axis: therapeutic targets for autoimmune inflammation" @default.
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• W2079494090 doi "https://doi.org/10.1016/j.coi.2006.09.008" @default.
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