Exposure to ultraviolet radiation (UVR) is one of major environmental factors that produce pleomorphic reactions in the whole organism and the skin. These include the well-described carcinogenic potential of UVR, the erythemogenic effects (sunburn), photoaging and suppression of cellular immune responses. Skin functions not only as an immune target organ but also as an immune effector organ. After exposure of the skin to noncytotoxic doses of UVB radiation, keratinocytes (KC), a major component of the epidermis, are directly or indirectly stimulated to express cytokines and other mediators such as prostaglandin E2, cis-urocanic acid, neuropeptides, and oxygen radicals. These factors are involved in the modulation of immune reactions. Such modulation of cutaneous and systemic immune responses by UVR has been examined by concentrating on the effects of UVR on cutaneous cellular components. Furthermore, an attempt has been made to investigate the effect of UVA on UVB-induced immune suppression by examining the production of cytokines from KC exposed to UVA. Although UVA seems to play an important role in suppressing immune reactions, UVA exposure after UVB irradiation has been shown to reverse UVB-induced suppression of contact hypersensitivity in mice. Our study showed that KC-derived IL-10 and IL-12 are regulated differentially by UVA and UVB. UVA (less than 20 kJ/m2) induced IL-12, a potent antagonist to UVB-induced immune suppression, but not IL-10, a Th2 cytokine responsible for the suppressed CHS by UVB. Our findings suggest that UVA seems to have a complex role in regulating the immune response by modulating cytokine profiles in the skin.