For therapeutic medical, cosmetic, and recreational reasons, humans expose themselves to increasing amounts of UVA. However, little is known of the photobiologic events associated with cutaneous carcinogenesis and photoaging that occur as a result of UVA exposure. UVB exposure of human skin abrogates the function of epidermal CD1+DR+ Langerhans cells and induces the appearance of CD1-DR+ non-Langerhans cell APC. This non-Langerhans cell APC population activates autoreactive immunoregulatory T cells that lead to suppressor-effector T cell function. In this report we show that, similarly to UBV, UVA exposure abrogates the function of CD1+DR+ Langerhans cells. However, in contrast to UVB, there is rapid recovery of Langerhans cell antigen-presenting cell activity and that CD1-DR+ non-Langerhans cell APC failed to appear to a significant degree. In keeping with the lack of CD1-DR+ epidermal cells, UVA exposed epidermal cells harvested 3 days after exposure functioned similarly to normal epidermis in that they activated alloreactive T cells but not autoreactive T cells in the absence of added Ag. This was in contrast to UVB irradiated epidermal cells that potently activate autoreactive T cells and contain CD1-DR+ cells. Thus, although both UVA and UVB initially depletes and inactivates CD1+DR+ Langerhans cells, the subsequent APC function of epidermal cells exposed to UVA differ profoundly from that of cells exposed to UVB. UVA radiation is less carcinogenic than UVB; differences in host responses to UV tumors may be linked to the rapid recovery of Langerhans cell function and the lack of induction of CD1-DR+ non-Langerhans cell APC after UVA exposure.