From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited.
From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited.
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DOI：
10.1111/j.1600-065x.2008.00714.x
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发表时间：
2008-12
影响因子：
8.7
通讯作者：
de Waal Malefyt R
中科院分区：
文献类型：
--
作者：
Boniface K;Blom B;Liu YJ;de Waal Malefyt R
导致效应 T 细胞反应失调的持续炎症是多种自身免疫性疾病的共同特征。白介素 12 (IL-12)/T 辅助细胞 1 (Th1) 通路被认为是多种慢性炎症性疾病的发病机制，包括牛皮癣、炎症性肠病、关节炎或多发性硬化症，主要是通过产生干扰素 γ 及其对巨噬细胞活化和趋化因子产生的影响。然而，随着 IL-12 相关细胞因子（称为 IL-23）的发现，T 细胞介导的慢性炎症的最初概念需要进行调整。 IL-23 因其参与慢性炎症的建立和产生 IL-17 的 Th 细胞亚群（称为 Th17）的发育而迅速得到认可，它与之前报道的 Th1 和 Th2 群体不同。本综述旨在描述 IL-23 及其受体的特征、其生物活性以及其在人类 Th17 细胞发育和自身免疫中的作用。
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.