Innate immune sensors stimulate inflammatory and immunosuppressive responses to UVB radiation.
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.
Division of Dermatology, Department of Medicine, University of California, San Diego and Veterans Affairs San Diego Health Care System, San Diego, California, USA.
Richard L
RL
Gallo
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.
Jamie J
JJ
Bernard
D000818:Animals; D004249:DNA Damage / Q000528:radiation effects*; D004260:DNA Repair; D005260:Female; D051197:Toll-Like Receptor 4 / Q000235:genetics* / Q000378:metabolism*
C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4