Article: article from journal or magazin.
The inflammasome mediates UVB-induced activation and secretion of interleukin-1beta by keratinocytes.
Journal Article Research Support, Non-U.S. Gov't --- Old month value: Jul 3
It has long been known that human keratinocytes are a potent source of the proinflammatory cytokines proIL-1alpha and -1beta, which are activated and released in response to UV irradiation . 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 Ca(2+) is required for activation of the IL-1beta-converting enzyme caspase-1 by the inflammasome, a multiprotein innate immune complex [3, 4]. Caspase-1 in turn activates proIL-1beta, and keratinocytes secrete the cytokine as well as inflammasome components. These results demonstrate the presence of a proIL-1beta-processing inflammasome in nonprofessional immune cells and the necessity of inflammasome components for the UVB-induced secretion of IL-1beta. This supports the concept that keratinocytes are important immuno-competent cells under physiological and pathological conditions .
Animals, Calcium/metabolism, Caspase 1/metabolism, Cytokines/metabolism, Cytokines/secretion, Cytoplasm/metabolism, Dermatitis/metabolism, Humans, Inflammation Mediators/metabolism, Interleukin-1/metabolism, Interleukin-1beta/metabolism, Interleukin-1beta/secretion, Keratinocytes/metabolism, Keratinocytes/radiation effects, Mice, Mice, Knockout, Multiprotein Complexes/metabolism, Protein Precursors/metabolism, Ultraviolet Rays
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