title: IL-23: one cytokine in control of autoimmunity.
abstract: During the past decade, it has been firmly established that IL-23 is essential for disease development in several models of autoimmune disease, including psoriatic skin inflammation, inflammatory bowel disease (IBD), and experimental autoimmune encephalomyelitis (EAE). The mechanism by which IL-23 exerts its pathogenic role has been mostly scrutinized in the context of Th17 cells, which were thought to mediate autoimmunity by secretion of IL-17 family cytokines. However, the picture emerging now is one of multiple IL-23-responsive cell types, pro-inflammatory cytokine induction, and pathogenic "licensing" following an IL-23-dominated interaction between the T cell and the antigen-presenting cell (APC). This review will focus on our changing view of IL-23-dependent autoimmune pathologies with a particular emphasis on the responder cells and their IL-23-induced factors that ultimately mediate tissue destruction.
authors.affiliation: Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
authors.forename: Andrew L
authors.initials: AL
authors.lastname: Croxford
authors.forename: Florian
authors.initials: F
authors.lastname: Mair
authors.forename: Burkhard
authors.initials: B
authors.lastname: Becher
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D015551:Autoimmunity / Q000276:immunology*; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology; D053759:Interleukin-23 / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D053759:Interleukin-23