Studies of delayed systemic effects of ultraviolet B radiation (UVR) on the induction of contact hypersensitivity, 2. Evidence that interleukin-10 from UVR-treated epidermis is the critical mediator

Acute, low-dose ultraviolet B radiation (UVR) alters cutaneous immunity at the local site as well as systemically. Within 2-3 days of UVR exposure, re cipient mice lose their capacity to develop contact hypersensitivity (CH) w hen hapten is painted on unexposed skin. This loss correlates temporally wi th a functional deficit among dendritic antigen-presenting cells within non -draining lymph nodes and spleen. In the experiments described, the delayed systemic immune deficiency following acute, low-dose UVR exposure was foun d to be eliminated with neutralizing anti interleukin-10 (IL-10) antibody. Intracutaneous injection of IL-10 generated a deficiency of systemic immuni ty as well as a functional deficit among lymph node dendritic cells that wa s similar to that induced by UVR. The skin itself was found to be the sourc e of the IL-10 responsible for these defects? and epidermis (presumably ker atinocytes) rather than mast cells was round to be the source of IL-10 with in UVR-exposed skin. The potential relationships are discussed between the delayed systemic immune deficit created by acute, low-dose UVR, and the sys temic immune deficits caused by chronic, high-dose UVR and by a single, hig h-dose UVR exposure.