Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of antibodies to components of the cell nucleus in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. The exact aetiology of SLE is unknown. SLE shows a strong familial aggregation, with a much higher frequency among first degree relatives of patients. Moreover, in extended families, SLE may coexist with other organ specific autoimmune diseases such as haemolytic anaemia, immune thrombocytopenic purpura, and thyroiditis. The concordance of the disease in identical twins is approximately 25–50% and that in dizygotic twins is around 5%.1 This suggests that genetic factors play an important role in the predisposition of the disease. However, most cases of SLE are sporadic without identifiable genetic predisposing factors, suggesting that multiple environmental or yet unknown factors may also be responsible.
