IL‐23: One cytokine in control of autoimmunity

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.