Photoimmunology

In vivo exposure of experimental animals and humans to UV radiation, with and without the addition of photosensitizers, can alter immune responses and the function and distribution of components of the immune system. In mice, exposure to UVB (290–320 nm) radiation suppresses delayed hypersensitivity (DH) responses such as allergic contact dermatitis to simple chemicals. The mechanism of this effect of radiation involves an alteration of the function of antigen-presenting cells, possibly Langerhans cells, resulting in the preferential induction of suppressor cells; the effect is mainly exerted on the induction phase of the immune response. In the guinea pig, exposure to either UVB or methoxsalen/UVA (PUVA) radiation suppresses allergic contact dermatitis and DH to hapten-protein conjugates. There is suggestive evidence that UV radiation may also suppress cutaneous DH responses in humans. Exposure to UV radiation can alter the function and viability of peripheral blood lymphocytes in humans. Following in vitro exposure, these effects are both dose- and wavelength-dependent. In vivo exposure to either UVB or PUVA radiation produces alterations in the function of circulating lymphocytes; the significance and long-term effects of these alterations have not been explored. There is increasing evidence that the effects of UVB and PUVA on immune function may be qualitatively different. For example, a single exposure of UVB radiation in humans produces a suppression of the response of lymphocytes following stimulation by phytohemagglutinin. Equi-erythemogenic doses of PUVA do not have this effect. Furthermore, in mice exposure to UVB radiation suppresses the normal immune response to UVB-induced skin tumors. In contrast, treatment with PUVA does not alter this immune response. These observations may be important to our understanding of the mechanisms underlying the beneficial and adverse effects of these 2 radiations