The inflammasome mediates UVB-Induced activation and secretion of interleukin-1β by keratinocytes
The inflammasome mediates UVB-Induced activation and secretion of interleukin-1β by keratinocytes
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DOI：
10.1016/j.cub.2007.05.074
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发表时间：
2007-07-03
期刊：
影响因子：
9.2
通讯作者：
Beer, Hans-Dietmar
中科院分区：
文献类型：
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作者：
Feldmeyer, Laurence;Keller, Martin;Beer, Hans-Dietmar
早就知道，人角质形成细胞是促炎性细胞因子proil -1α和-1β[1]的有效来源，它们是对紫外线照射的响应[2]的激活和释放的-1β[1]。然而，调节角质形成细胞中IL-1的成熟和分泌的细胞内途径尚不清楚。在这里，我们表明，UVB介导的细胞质Ca2+的增强是激活IL-1β-转换酶CASPase-Caspase-1的炎症体，这是一种多蛋白质的先天免疫复合物[3，4]。 caspase-1反过来激活了proil-1β，角质形成细胞分泌细胞因子以及炎症组成分。这些结果表明，非专业免疫细胞中存在proil-1β处理炎症体，以及对于UVB诱导的IL-1βββ的炎性组成分的必要性。这支持了角质形成细胞在生理和病理条件下是重要的免疫能力细胞[5]。
It has long been known that human keratinocytes are a potent source of the proinflammatory cytokines proIL-1 alpha and -1 beta [1], which are activated and released in response to UV irradiation [2]. However, the intracellular pathways, which regulate maturation and secretion of IL-1 in keratinocytes, are unknown. Here we show that the UVB-mediated enhancement of cytoplasmic Ca2+, is required for activation of the IL-1 beta-converting enzyme caspase-1 by the inflammasome, a multiprotein innate immune complex [3, 4]. Caspase-1 in turn activates proIL-1 beta, and keratinocytes secrete the cytokine as well as inflammasome components. These results demonstrate the presence of a proIL-1 beta-processing inflammasome in nonprofessional immune cells and the necessity of inflammasome components for the UVB-induced secretion of IL-1 beta. This supports the concept that keratinocytes are important immunocompetent cells under physiological and pathological conditions [5].