Langerhans cells orchestrate apoptosis of DNA‐damaged keratinocytes upon high‐dose UVB skin exposure Article Swipe
Daniela Ortner
,
Helen Strandt
,
Christoph H. Tripp
,
Sarah Spoeck
,
Athanasios Seretis
,
Florian Hornsteiner
,
Sophie Dieckmann
,
Matthias Schmuth
,
Patrizia Stoitzner
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1002/eji.202451020
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1002/eji.202451020
Ultraviolet (UV) irradiation of the skin causes mutations that can promote the development of melanoma and nonmelanoma skin cancer. High‐dose UVB exposure triggers a vigorous skin reaction characterized by inflammation resulting in acute sunburn. This response includes the formation of sunburn cells and keratinocytes (KC) undergoing programmed cell death (apoptosis) when repair mechanisms of DNA damage are inadequate. The primary objective of this research was to clarify the involvement of Langerhans cells (LC) in the development of acute sunburn following intense UVB skin irradiation. To address this, we subjected the dorsal skin of mice to a single high‐dose UVB exposure and analyzed the immediate immune response occurring within the skin tissue. Acute sunburn triggered an activation of LC, coinciding with a rapid influx of neutrophils that produced TNF‐α. Furthermore, our investigation unveiled a marked increase in DNA‐damaged KC and the subsequent induction of apoptosis in these cells. Importantly, we demonstrate a crucial link between the inflammatory cascade, the initiation of apoptosis in DNA‐damaged KC, and the presence of LC in the skin. LC were observed to modulate the chemokine response in the skin following exposure to UVB, thereby affecting the trafficking of neutrophils. Skin lacking LC revealed diminished inflammation, contained fewer TNF‐α‐producing neutrophils, and due to the prevention of apoptosis induction, a lingering population of DNA‐damaged KC, presumably carrying the risk of enduring genomic alterations. In summary, our results underscore the pivotal role of LC in preserving the homeostasis of UVB‐irradiated skin. These findings contribute to a deeper understanding of the intricate mechanisms underlying acute sunburn responses and their implications for UV‐induced skin cancer.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/eji.202451020
- OA Status
- hybrid
- Cited By
- 7
- References
- 57
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4402568310
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4402568310Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1002/eji.202451020Digital Object Identifier
- Title
-
Langerhans cells orchestrate apoptosis of DNA‐damaged keratinocytes upon high‐dose UVB skin exposureWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-09-17Full publication date if available
- Authors
-
Daniela Ortner, Helen Strandt, Christoph H. Tripp, Sarah Spoeck, Athanasios Seretis, Florian Hornsteiner, Sophie Dieckmann, Matthias Schmuth, Patrizia StoitznerList of authors in order
- Landing page
-
https://doi.org/10.1002/eji.202451020Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
hybridOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1002/eji.202451020Direct OA link when available
- Concepts
-
Sunburn, Apoptosis, Skin cancer, DNA damage, Biology, UVB-induced apoptosis, Inflammation, Chemokine, Programmed cell death, Immunology, Tumor necrosis factor alpha, Cancer research, Melanoma, Necrosis, Immune system, Cell biology, DNA, Cancer, Caspase, Medicine, Dermatology, GeneticsTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
7Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 6, 2024: 1Per-year citation counts (last 5 years)
- References (count)
-
57Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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