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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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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2014
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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. |
format | Online Article Text |
id | pubmed-4133277 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
record_format | MEDLINE/PubMed |
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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