Although for decades sunlight was suspected to be involved in the development of cutaneous lupus erythematosus (CLE), only in recent years research on the effects of ultraviolet irradiation on the skin of patients with CLE has resulted in a more comprehensive model for the pathogenesis of the disease. In this model, exposure to UV light induces apoptosis of keratinocytes and the release of pro-inflammatory cytokines. In susceptible patients, the presence or even accumulation of apoptotic cells results in the induction of characteristic inflammatory skin lesions, which might be due to a delayed and pro-inflammatory clearance of these apoptotic cells. Many other factors, in part genetically determined, are involved in CLE resulting in a very heterogeneous clinical manifestation. Among these factors, presence of autoantibodies, a decreased number of regulatory T cells at the site of inflammation and increased expression of pro-inflammatory cytokines like TNFalpha and IFN-inducible protein myxovirus protein A have been shown to play a role in the pathogenesis of CLE.