Caucasians are surprisingly prone to sunburn. Ultraviolet radiation within the UVB bandwidth causes photochemical alterations in both the DNA and membrane lipids of epidermal cells (Halliday, 2005). Furthermore, low doses of UVB appear to coordinately suppress keratinocyte proliferation and stimulate cellular maturation. Surprisingly, low doses of UVB also suppress certain arms of the adaptive immune system (Halliday, 2005). For example, UVB treatment depresses acute and delayed hypersensitivity reactions. Certain chronic inflammatory skin conditions, such as psoriasis, are treated with measured doses of UVB, in part for this reason. UVB is believed to cause immunosuppression by direct action on immune cells within the skin, as well as indirectly. Vitamin D, converted by UVB in skin from 7DHC has potent immunosuppressant properties. Indeed, the active forms of Vitamin D have been shown to inhibit T cell proliferation, inhibit expression of MHC class II proteins on antigen presenting cells, and depress the activity of Langerhans cells (Lehmann et al, 2004). In addition, sunlight stimulates the keratinocyte and the melanocyte to express alphaMSH, a hormone that not only plays a role in the pigmentation of skin but also serves to suppress epidermal inflammation (Brogden et al, 2005).
Thus, sunlight, which so readily damages skin normally, also "quiets" the adaptive immune system within the skin, in part through the activation of the Vitamin D signaling pathway. We presume that without the induction of UVB-associated immunosuppression we would suffer severe inflammation following "normal" exposure to sunlight. The reports by Mallbris et al, Weber et al, and Wang et al tell us that while the adaptive system is being "toned down", UVB, via the Vitamin D pathway, also causes a "non-inflammatory" antimicrobial component of the innate immune system to be "turned on".
