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

Abstract

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