From interleukin‐23 to T‐helper 17 cells: human T‐helper cell differentiation revisited

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Abstract
Summary: Protracted inflammation leading to dysregulation of effector T‐cell responses represents a common feature of a wide range of autoimmune diseases. The interleukin‐12 (IL‐12)/T‐helper 1 (Th1) pathway was thought to be responsible for the pathogenesis of multiple chronic inflammatory diseases, including psoriasis, inflammatory bowel disease, arthritis, or multiple sclerosis, mainly through their production of interferon‐γ and its effects on macrophage activation and chemokine production. However, this initial concept of T‐cell‐mediated chronic inflammation required an adjustment with the discovery of an IL‐12‐related cytokine, designated IL‐23. IL‐23 was rapidly recognized for its involvement in the establishment of chronic inflammation and in the development of a Th cell subset producing IL‐17, designated Th17, which is distinct from the previously reported Th1 and Th2 populations. This review aims to describe the characterization of IL‐23 and its receptor, its biological activities, as well as its involvement in the development of human Th17 cells and autoimmunity.