In the human body, every day billions of apoptotic cells are produced. Removal of these cells is necessary, to prevent the release of intracellular toxic constituents, and occurs very effectively via phagocytosis by (semi)-professional phagocytes. This elimination process occurs rapidly and without inflammation. In systemic lupus erythematosus (SLE) a disturbed elimination of apoptotic cells has been implicated in the induction and reactivation of the disease. Accumulation of apoptotic cells may result in autoantibody formation. A delayed, pro-inflammatory clearance is also thought to play a crucial role in the development of inflammatory lesions once the disease has manifested. One of the hallmarks of patients with SLE is the development of cutaneous lesions upon exposure to sunlight. In this review, we will focus on apoptotic cells, their elimination, and the consequences of a disturbed elimination of apoptotic cells on the development of UVB induced inflammatory skin lesions.