title: The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation.
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.
authors.affiliation: Eli Lilly and Company, Indianapolis, IN 46285, USA.
authors.forename: Kristine
authors.initials: K
authors.lastname: Kikly
authors.forename: Ling
authors.initials: L
authors.lastname: Liu
authors.forename: Songqing
authors.initials: S
authors.lastname: Na
authors.forename: Jonathon D
authors.initials: JD
authors.lastname: Sedgwick
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology; D053759:Interleukin-23 / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D053759:Interleukin-23