Ultraviolet radiation (UVR)-induced immunosuppression and genetic mutations are responsible for skin carcinogenesis. To study UV-induced immunosuppression we recruit human volunteers who have memory responses to nickel or tuberculin purified protein derivative. Recently, using narrow band interference filters, we have determined the wavelength dependence for UV immunosuppression in humans. There are two distinct wavebands in terrestrial sunlight that cause immunosuppression, one centered at about 310 nm (UVB), the other at 370 nm (upper UVA). UVB immunosuppression likely results from genetic damage (cyclobutane pyrimidine dimers). The similarity of the UVA waveband response to formation of reactive oxygen species (ROS) and oxidative damage to DNA (8-oxo-7,8-dihydro-2’-deoxyguanosine) suggests that UV-induced ROS may be one mediator of UVA immunosuppression. Other mechanisms that we have identified to be involved in UV immunosuppression include activation of the alternative complement pathway, activation of B suppressor lymphocytes, inhibition of T effector cell activation, modulation of chemokines, cytokines and mast cells. A key central mechanism is glycolytic blockade and reduced ATP levels. This UV-induced energy crisis in skin cells can be prevented with topical or oral nicotinamide (vitamin B3). Nicotinamide is a precursor of NAD and an essential cofactor in the production of ATP. Nicotinamide enhances DNA repair, reducing the levels of UV-induced genetic damage. Nicotinamide also protects humans from UV-induced immunosuppression. Modulation of bioenergetics in the skin, by using nicotinamide to prevent the UV-induced energy crisis, is an effective form of suncare.