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Ultraviolet B radiation illuminates the role of TLR3 in the epidermis

UV radiation poses a significant risk to human health. The mechanisms that help repair UV-damaged cells have recently been more clearly defined with the observation that Toll-like receptor 3 can sense self RNA released from necrotic keratinocytes following UV damage. TLR3 activation in the skin indu...

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Detalles Bibliográficos
Autores principales: Borkowski, Andrew W., Gallo, Richard L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133277/
https://www.ncbi.nlm.nih.gov/pubmed/24786223
http://dx.doi.org/10.1038/jid.2014.167
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author Borkowski, Andrew W.
Gallo, Richard L.
author_facet Borkowski, Andrew W.
Gallo, Richard L.
author_sort Borkowski, Andrew W.
collection PubMed
description UV radiation poses a significant risk to human health. The mechanisms that help repair UV-damaged cells have recently been more clearly defined with the observation that Toll-like receptor 3 can sense self RNA released from necrotic keratinocytes following UV damage. TLR3 activation in the skin induces inflammation and increases expression of genes involved in skin barrier repair. Activation of TLR2 in the skin by commensal microbial products prevents excessive inflammation by blocking downstream TLR3 signaling. This review highlights how UV damage induced inflammation in the skin is propagated by host products and regulated by host inhabitants.
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spelling pubmed-41332772015-03-01 Ultraviolet B radiation illuminates the role of TLR3 in the epidermis Borkowski, Andrew W. Gallo, Richard L. J Invest Dermatol Article UV radiation poses a significant risk to human health. The mechanisms that help repair UV-damaged cells have recently been more clearly defined with the observation that Toll-like receptor 3 can sense self RNA released from necrotic keratinocytes following UV damage. TLR3 activation in the skin induces inflammation and increases expression of genes involved in skin barrier repair. Activation of TLR2 in the skin by commensal microbial products prevents excessive inflammation by blocking downstream TLR3 signaling. This review highlights how UV damage induced inflammation in the skin is propagated by host products and regulated by host inhabitants. 2014-05-01 2014-09 /pmc/articles/PMC4133277/ /pubmed/24786223 http://dx.doi.org/10.1038/jid.2014.167 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Borkowski, Andrew W.
Gallo, Richard L.
Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title_full Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title_fullStr Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title_full_unstemmed Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title_short Ultraviolet B radiation illuminates the role of TLR3 in the epidermis
title_sort ultraviolet b radiation illuminates the role of tlr3 in the epidermis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133277/
https://www.ncbi.nlm.nih.gov/pubmed/24786223
http://dx.doi.org/10.1038/jid.2014.167
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