IL-33 is regulated by TNF-α in normal and psoriatic skin
IL-33 is regulated by TNF-α in normal and psoriatic skin
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DOI：
10.1007/s00403-014-1447-9
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发表时间：
2014-04-01
影响因子：
3
通讯作者：
Ayala, Fabio
中科院分区：
文献类型：
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作者：
Balato, Anna;Di Caprio, Roberta;Ayala, Fabio
白细胞介素-33（IL-33）是最近发现的IL-1家族成员。IL-33被认为是坏死细胞响应于组织损伤或损害而释放的内源性“alarmin”，在暴露于环境的组织中组成型表达，其中内皮细胞和上皮细胞构成其主要来源。一些发现报道了促炎刺激物，如IFN-γ和TNF-α，以及IL-17，可以诱导正常人表皮角质形成细胞中的IL-33表达。在本研究中，我们深入研究了IL-33和TNF-α之间的关系，采用整个皮肤作为研究模型。TNF-α剂量和时间依赖性地诱导离体健康皮肤器官培养物中IL-33基因表达类似地，TNF-α显著增加正常人表皮片中IL-33 mRNA的表达。此外，IL-33在银屑病皮肤中增强，抗TNF-α治疗能够显著降低IL-33的生物学复杂性增加，现在已知该分子具有超出其原始描述的额外作用。特别是，我们可以评估IL-33在正常和银屑病皮肤中受TNF-α调节。
Interleukin-33 (IL-33) is the most recently discovered IL-1 family member. Considered an endogenous "alarmin" released by necrotic cells in response to tissue injury or damage, IL-33 is constitutively expressed in tissues exposed to the environment, where endothelial and epithelial cells constitute its major sources. Several findings reported that pro-inflammatory stimuli, such as IFN-gamma and TNF-alpha, as well as IL-17, can induce IL-33 expression in normal human epidermal keratinocytes. In the present study, we deeply investigated the relation between IL-33 and TNF-alpha, by employing the whole skin as study model. TNF-alpha dose- and time-dependently induced IL-33 gene expression in ex vivo healthy skin organ culture. Similarly, TNF-alpha significantly increased IL-33 mRNA expression in normal human epidermal sheets. Moreover, IL-33 was enhanced in psoriatic skin and anti-TNF-alpha therapy was able to significantly reduce it. The biology of IL-33 is gaining in complexity, and this molecule is now known to have additional roles beyond its original description. In particular, we can assess that IL-33 is regulated by TNF-alpha in normal and psoriatic skin.