The role of IL-23 and the IL-23/T(H) 17 immune axis in the pathogenesis and treatment of psoriasis.
The role of IL-23 and the IL-23/T(H) 17 immune axis in the pathogenesis and treatment of psoriasis.
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DOI：
10.1111/jdv.14433
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发表时间：
2017-10
期刊：
影响因子：
--
通讯作者：
Prinz JC
中科院分区：
文献类型：
--
作者：
Girolomoni G;Strohal R;Puig L;Bachelez H;Barker J;Boehncke WH;Prinz JC
牛皮癣是一种慢性免疫介导疾病，影响全球超过1亿人，占英国人口的2.2%。牛皮癣的病因被认为是遗传、环境、感染和生活方式等因素相互作用的结果。遗传和环境因素相互作用导致分子疾病机制的方式仍然难以捉摸。然而，白细胞介素23 (IL‐23)/辅助性T‐17 （TH17）免疫轴已被确定为银屑病发病机制的主要免疫途径。该途径的核心是细胞因子IL‐23，它是一种异源二聚体，由IL‐12中也发现的p40亚基和IL‐23独有的p19亚基组成。IL‐23对于维持TH17反应很重要，与非病变皮肤相比，银屑病皮肤中IL‐23水平升高。目前，许多特异性抑制IL - 23p19的药物正在开发中，用于治疗中至重度斑块型银屑病，最近的临床试验证明其具有良好的安全性和耐受性。这些数据支持该细胞因子在牛皮癣发病机制中的作用。更好地了解IL - 23/TH17免疫轴是至关重要的，并将促进银屑病和其他具有相似遗传病因和发病途径的炎症性疾病的其他靶点的发展。
Psoriasis is a chronic, immune‐mediated disease affecting more than 100 million people worldwide and up to 2.2% of the UK population. The aetiology of psoriasis is thought to originate from an interplay of genetic, environmental, infectious and lifestyle factors. The manner in which genetic and environmental factors interact to contribute to the molecular disease mechanisms has remained elusive. However, the interleukin 23 (IL‐23)/T‐helper 17 (TH17) immune axis has been identified as a major immune pathway in psoriasis disease pathogenesis. Central to this pathway is the cytokine IL‐23, a heterodimer composed of a p40 subunit also found in IL‐12 and a p19 subunit exclusive to IL‐23. IL‐23 is important for maintaining TH17 responses, and levels of IL‐23 are elevated in psoriatic skin compared with non‐lesional skin. A number of agents that specifically inhibit IL‐23p19 are currently in development for the treatment of moderate‐to‐severe plaque psoriasis, with recent clinical trials demonstrating efficacy with a good safety and tolerability profile. These data support the role of this cytokine in the pathogenesis of psoriasis. A better understanding of the IL‐23/TH17 immune axis is vital and will promote the development of additional targets for psoriasis and other inflammatory diseases that share similar genetic aetiology and pathogenetic pathways.
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影响因子：
82.9
作者：
Conrad, Curdin;Boyman, Onur;Nestle, Frank O.
通讯作者：
Nestle, Frank O.
影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
影响因子：
9.8
作者：
Cargill, Michele;Schrodi, Steven J.;Begovich, Ann B.
通讯作者：
Begovich, Ann B.
DOI：
10.1084/jem.20060244
发表时间：
2006-11-27
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Chan JR;Blumenschein W;Murphy E;Diveu C;Wiekowski M;Abbondanzo S;Lucian L;Geissler R;Brodie S;Kimball AB;Gorman DM;Smith K;de Waal Malefyt R;Kastelein RA;McClanahan TK;Bowman EP
通讯作者：
Bowman EP
影响因子：
3.5
作者：
Capon, Francesca;Bijlmakers, Marie-Jose;Trembath, Richard C.
通讯作者：
Trembath, Richard C.