The deleterious effects of ultraviolet B radiation (UVR) on cutaneous immunity are mediated in part by cytokines released from cutaneous cells following radiation exposure. On the one hand, TNF‐α has been advocated as the primary mediator of failed contact hypersensitivity induction, and, on the other hand, IL‐10 has been held responsible for tolerance. While keratinocytes exposed toUVR have been found to produce both TNF‐α and IL‐10, there is reason to question whether these major cellular constituents of the epidermis are the relevant source of immunomodulatory cytokinesafter UVR. Dermal mast cells also produce TNF‐α and IL‐10, and we have recently reported that mast cell‐derived TNF‐α is required for UVR‐induced impairment of CH induction. In this study, we have examined whether mast cells are also a relevant source of IL‐10 in UVR‐dependent tolerance. We found that (a) UVR fails to induce tolerance in mast cell‐deficient mice, and (b) that tolerance occurs if mast cells are triggered to degranulate after ligation of the IgE receptor. Both types of tolerance were neutralized with anti‐IL‐10 antibodies, are hapten specific, and are associated with regulatory lymphoid cells. We conclude that mast cells are required in UVR‐induced tolerance and may be one of the major sources of IL‐10 that mediates the tolerance induced by acute, low‐dose UVR.