 The phenomenon of UVR-induced immunosuppression suppression of CHS has been well known for many years. Recent findings showed that regulatory T cells CD4CD25FoxP3 Tregs, a subset of T helper cells, are crucial in UVR-induced immunosuppression. However, the requirements for the maintenance of peripheral CD4CD25 T cells, important in suppression of immune responses, are still incompletely understood. Recent work suggests that cutaneous RANKL might be the physiologic missing link that couples UVR to immunosuppression. Epidermal RANKL, expressed in keratinocytes of inflamed skin due to e.g. UVR exposure was shown to control the number of Tregs via activation of dendritic cells, hereby mediating UVR-induced immunosuppression e.g. suppression of allergic contact hypersensitivity responses. In addition to the suppression of local cutaneous hyperallergic responses, the development of systemic autoimmunity is suppressed. A strong inducer of RANKL expression and of Tregs is vitamin D3 that has been reported to have immunosuppressive effects. Interestingly, patients with autoimmune disorders e.g. lupus erythematosus may exhibit reduced vitamin D3 blood levels. 