Narrowband UVB and Solar-Simulated UV Suppress Systemic Immune Responses through Different Mechanisms.

Abstract

UV-induced immune suppression contributes to skin carcinogenesis and may also explain how sunlight protects against nonskin autoimmune diseases, particularly multiple sclerosis. Narrowband UVB (NBUVB) phototherapy is an effective treatment for some skin diseases; however, its mechanism of action and its potential for treating diseases away from the skin are not well-understood. Solar-simulated UV modulates immune cells, in part, by altering lipids. However, whether NBUVB has the same effect on these cells and molecules is unknown. Exposure of mice to an immunosuppressive dose of NBUVB did not affect plasma lipid levels, which were altered after solar-simulated UV irradiation. Surprisingly, unlike what occurs after solar-simulated UV irradiation, dermal mast cells and lymphocyte recirculation were unaffected by NBUVB. NBUVB-irradiated skin showed a reduced number of epidermal CD207⁺ cells and cutaneous CD3⁺ T cells, and was infiltrated by Ly6G⁺ neutrophils. There was also an increase in the number of CD4⁺FoxP3⁺ T cells in the skin-draining lymph nodes and suppression of antigen-specific CD8⁺ T-cell activity in vivo. Thus, immunosuppressive NBUVB activates some but not all the pathways responsible for the immunosuppressive effects of solar-simulated UV. Understanding the wavelength-dependent effects of UVR on the immune system is essential to harness its immunomodulatory capacity to treat a wide range of diseases.