The IL-23/Th17 axis: therapeutic targets for autoimmune inflammation

Autoimmune inflammatory responses and the diseases that develop as a consequence are now thought to be driven through a novel non-Th1 pathway. IL-23, together with additional factors including TGF-β1 and IL-6, collectively generate and sustain a distinct CD4+ ‘Th17 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/Th17 axis that are key to disease development.