A New Pathway for Solar Ultraviolet Skin Inflammation

UVB radiation damages noncoding RNA, affecting a receptor that is part of the innate immune system.

Sunburn, nonmelanoma skin cancer, melanoma, and immunosuppression are some deleterious effects of solar ultraviolet (UV) radiation. The biologic mechanisms by which UV radiation exerts these diverse actions have not been completely discovered. Investigators examined the roles of RNA and the toll-like receptor 3 (TLR3) in cutaneous effects of UVB radiation. The TLR3 receptor molecule, present on keratinocytes, is part of the innate immune system. In UVB-irradiated keratinocytes, RNA has been found to stimulate production of the inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin (IL)-6, thought to contribute to the UV-induced inflammatory response.

A comparison of RNA from UVB-irradiated and unirradiated keratinocytes showe…

Reviewing Author

Craig A. Elmets, MD

Disclosures

Consultant / Advisory board Astellas Pharmaceuticals

EquityVaxin

Grant / Research support NIH; NIH/NCI; Veteran’s Administration; Ferndale Laboratories; Kyowa Hakko Kirin Pharma, Inc.

Editorial boards Cancer Prevention Research; Photodermatology, Photoimmunology, & Photomedicine; UpToDate; eMedicine; Journal of Dermatological Sciences; JAMA Dermatology

Leadership positions in professional societies American Academy of Dermatology (Vice Chair, Committee on Science and Research); Photomedicine Society (Board of Directors)