Exposure to UV Wavelengths in Sunlight Suppresses Immunity. To What Extent is UV-induced Vitamin D3 the Mediator Responsible?

Abstract

Reduced immunity following exposure of skin to UV radiation (UVR) may explain the positive latitude gradient measured for a number of autoimmune diseases (greater incidence of disease with residence at higher latitudes), including multiple sclerosis, allergic asthma and diabetes. Humans obtain >80% of their vitamin D3 by exposure of skin to UVR in sunlight. In experimental models, both vitamin D3-dependent and vitamin D3-independent pathways have been implicated in the mechanisms of UVR-induced systemic suppression of immunity. However, where does the balance of control lie? How important is vitamin D3 other than providing a biomarker of sun exposure? Are other molecules/pathways activated by UVR more important? Murine and human studies suggest many molecules may play a role and their participation may vary with different diseases and the time of UVR exposure or vitamin D3 sufficiency/deficiency. Although low vitamin D3 levels have been associated with increased prevalence and progression of human autoimmune diseases, the benefits of supplementation with vitamin D3 have not been definitive. Vitamin D3 levels are a measure of past sun exposure but vitamin D3-dependent and vitamin D3-independent immunosuppressive effects of UVR may play a role in control of autoimmune diseases.