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首页> 外文期刊>Cell death and differentiation >Enhanced contact allergen- and UVB-induced keratinocyte apoptosis in the absence of CD95/Fas/Apo-1.
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Enhanced contact allergen- and UVB-induced keratinocyte apoptosis in the absence of CD95/Fas/Apo-1.

机译：在没有CD95 / Fas / Apo-1的情况下，增强的接触变应原和UVB诱导的角质形成细胞凋亡。

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摘要

FAS/CD95/Apo-1 is a ubiquitously expressed cell-surface receptor involved in the initiation of programmed cell death. Its function in epidermal keratinocytes has been incompletely defined. Available evidence from in vitro studies points to important roles of Fas in the pathogenesis of contact dermatitis and in keratinocyte apoptosis induced by ultraviolet light. To define functions of Fas in the epidermis in vivo, we have generated mice with epidermis-specific deletion of the fas gene and tested its requirement for 2,4-dinitrofluorobenzene-induced contact dermatitis and for ultraviolet light B (UVB)-induced keratinocyte apoptosis. We report here our unexpected finding that keratinocyte apoptosis induced by both a contact allergen and UVB irradiation was significantly enhanced in Fas-negative epidermis. Expression of Fas by epidermal keratinocytes was neither necessary for the normal development of contact hypersensitivity of the skin, nor required for keratinocyte apoptosis following UVB irradiation. Our study results thus show that in the epidermis in vivo Fas exerts antiapoptotic effects that outweigh its proapoptotic role in contact hypersensitivity responses of the skin and in the tissue response of the epidermis to UVB irradiation.
机译：FAS / CD95 / Apo-1是一种普遍表达的细胞表面受体，参与程序性细胞死亡的启动。在表皮角质形成细胞中的功能尚未完全定义。体外研究的现有证据表明，Fas在接触性皮炎的发病机理中以及在紫外线诱导的角质形成细胞凋亡中起着重要作用。为了定义Fas在体内表皮中的功能，我们已经生成了具有fas基因表皮特异性缺失的小鼠，并测试了其对2,4-二硝基氟苯诱导的接触性皮炎和紫外线B（UVB）诱导的角质形成细胞凋亡的需求。我们在这里报告了我们出乎意料的发现，即由接触性变应原和UVB辐射诱导的角质形成细胞凋亡在Fas阴性表皮中显着增强。表皮角质形成细胞表达Fas既不是正常的皮肤接触性超敏反应发展所必需的，也不是UVB照射后角质形成细胞凋亡所必需的。因此，我们的研究结果表明，Fas在体内表皮中发挥抗凋亡作用，其作用超过了皮肤接触性超敏反应以及表皮对UVB辐射的组织反应中的促凋亡作用。

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