IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis.
IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis.
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DOI：
10.1084/jem.20060244
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发表时间：
2006-11-27
期刊：
影响因子：
--
通讯作者：
Bowman EP
中科院分区：
文献类型：
--
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
细胞因子的异常表达被认为是银屑病的一个潜在原因，尽管目前还不清楚哪些细胞因子起关键作用。白细胞介素（IL）-23在人银屑病中表达，并且可能是主要调节细胞因子。在小鼠皮肤中直接皮内施用IL-23而不是IL-12，引发肿瘤坏死因子依赖性但IL-17 A非依赖性事件级联，导致红斑、混合性真皮浸润和与角化不全相关的表皮增生。IL-23诱导小鼠皮肤中IL-19和IL-24的表达，并且这两种基因在人类银屑病中也升高。在IL-19−/−和IL-24−/−小鼠中观察到IL-23依赖性表皮增生，但在IL-20 R2 −/−小鼠中受到抑制。这些数据暗示IL-23在银屑病的发病机制中，并支持IL-20 R2作为新的治疗靶点。
Aberrant cytokine expression has been proposed as an underlying cause of psoriasis, although it is unclear which cytokines play critical roles. Interleukin (IL)-23 is expressed in human psoriasis and may be a master regulator cytokine. Direct intradermal administration of IL-23 in mouse skin, but not IL-12, initiates a tumor necrosis factor–dependent, but IL-17A–independent, cascade of events resulting in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis. IL-23 induced IL-19 and IL-24 expression in mouse skin, and both genes were also elevated in human psoriasis. IL-23–dependent epidermal hyperplasia was observed in IL-19−/− and IL-24−/− mice, but was inhibited in IL-20R2−/− mice. These data implicate IL-23 in the pathogenesis of psoriasis and support IL-20R2 as a novel therapeutic target.
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