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The Inflammasome Mediates UVB-Induced Activation and Secretion of Interleukin-1β by Keratinocytes
Open accessAbstract
It has long been known that human keratinocytes are a potent source of the proinflammatory cytokines proIL-1alpha and -1beta[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 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 [5].
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“Recent studies have implicated the inflammasome, a multiprotein complex of the innate immune system responsible for activation and release of IL-1β from several skin cell types, in the development of chronic wounds (31, 32).”
From Wound repair and regeneration: Mechanisms, signaling, and translation (2014) · cites this paper as [31]
In the citing paper
“We postulated that constitutive expression of pro-IL-1β by keratinocytes [20] as shown (Figure 2A) would prime them for activation of the inflammasome.”
From Staphylococcus aureus activation of caspase 1/calpain signaling mediates invasion through human keratinocytes (2012) · cites this paper as [20]
In the citing paper
“For example, both murine and human keratinocytes express inflammasome components NLRP-3, ASC, caspase-1, IL-1β, and IL-18 (43,44).”
From Sustained Inflammasome Activity in Macrophages Impairs Wound Healing in Type 2 Diabetic Humans and Mice (2014) · cites this paper as [43]
In the citing paper
“In addition, ultraviolet irradiation–induced IL-1β secretion from human keratinocytes in vitro appears to be mediated by the NLRP-3 inflammasome (43)”
From Sustained Inflammasome Activity in Macrophages Impairs Wound Healing in Type 2 Diabetic Humans and Mice (2014) · cites this paper as [43]
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Metadata
- Authors
- Feldmeyer, L., Keller, M., Niklaus, G., Hohl, D., Werner, S., & Beer, H.-D.
- Affiliations
- ETH Zurich (CH)
- Centre Hospitalier Universitaire Vaudois (CH)
- Corresponding author
- Beer, Hans-Dietmar
- Venue
- Current Biology
- Publisher
- Elsevier BV
- Published
- 2007-07
- Volume
- 17
- Issue
- 13
- Pages
- 1140-1145
- ISSN
- 0960-9822 (ISSN-L)
- OpenAlex
- W1999276471
- Cited by
- 544
- References
- 25
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 19 · 2023: 22 · 2022: 23 · 2021: 32 · 2020: 29 · 2019: 30 · 2018: 30 · 2017: 38 · 2016: 34 · 2015: 35 · 2014: 40 · 2013: 30 · 2012: 41
- FWCI
- 10.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Current Biology (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Keywords
- inflammasome, UVB irradiation, IL-1β, keratinocytes, caspase-1, intracellular calcium, innate immunity, skin inflammation
- MeSH terms
- Animals, Calcium, Cytoplasm, Dermatitis, Humans, Interleukin-1, Protein Precursors, Ultraviolet Rays, Keratinocytes, Cytokines, Mice, Knockout, Inflammation Mediators, Caspase 1, Multiprotein Complexes, Mice, Interleukin-1beta
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