Systemic lupus erythematosus (SLE) is an organ non-specific autoimmune disorder, with multiple immunopathogenic mechanisms being implicated in its development. The most conspicuous feature of the disease is an exaggerated synthesis of various types of autoantibodies, followed by the formation of immune complexes that deposit in tissues and elicit an inflammatory response. Apart from antibodies, dendritic cells, T cells and cytokines are substantially involved in the pathogenesis of SLE and class I interferons seem to play a crucial role. SLE is a genetically determined disease. HLA system and complement system genes, apoptosis regulating genes and IgG Fc-gamma receptor genes are among the multiple genes implicated in SLE. The role of hormones, both estrogen and progesterone, in SLE activity has been reported. Some monoclonal antibodies have recently proved effective in the treatment of SLE.