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J Invest Dermatol. 2014 Jun;134(6):1508-1511. doi: 10.1038/jid.2014.32.

Innate immune sensors stimulate inflammatory and immunosuppressive responses to UVB radiation.

Author information

1
Division of Dermatology, Department of Medicine, University of California, San Diego and Veterans Affairs San Diego Health Care System, San Diego, California, USA.
2
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA. Electronic address: jjb313@rci.rutgers.edu.

Abstract

Almost 40 years from when it was first reported that UVB radiation exposure would modulate immune signaling, the photoimmunology field is still trying to understand the mechanisms by which UVB initiates inflammatory responses and modulates immune recognition. This commentary focuses on the ability of Toll-like receptors (TLRs), specifically TLR4 (Ahmad et al., 2014) and ligands such as damage-associated molecular patterns (DAMPs) released from injured cells to stimulate innate immune signaling and inflammatory cytokine production following UVB irradiation.

PMID:
24825061
PMCID:
PMC4271625
DOI:
10.1038/jid.2014.32
[Indexed for MEDLINE]
Free PMC Article

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