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, recipient mice lose their capacity to develop contact hypersensitivity (CH) when hapten is painted on unexposed skin. This loss correlates temporally with 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 found to be eliminated with neutralizing anti‐interleukin‐10 (IL‐10) antibody. Intracutaneous injection of IL‐10 generated a deficiency of systemic immunity as well as a functional deficit among lymph node dendritic cells that was similar to that induced by UVR. The skin itself was found to be the source of the IL‐10 responsible for these defects, and epidermis (presumably keratinocytes) rather than mast cells was found to be the source of IL‐10 within UVR‐exposed skin. The potential relationships are discussed between the delayed systemic immune deficit created by acute, low‐dose UVR, and the systemic immune deficits caused by chronic, high‐dose UVR and by a single, high‐dose UVR exposure.