Updating on the pathogenesis of systemic lupus erythematosus
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%.
Table 1 summarises the genes that are involved in human SLE. The female predilection becomes less pronounced outside the reproductive age range.
Although the etiology of systemic lupus erythematosus is unknown, recent studies have shed light on the pathoge-netic pathways that lead to tissue damage.
The immune system in systemic lupus erythematosus is characterized by a complex interplay between overactive B cells, abnormally activated T cells, and antigen-presenting cells.
In addition, many polymorphic non-MHC genes have been reported to be associated with SLE.
These include genes that encode mannose binding protein (MBP), tumour necrosis factor α, the T cell receptor, interleukin 6 (IL-6), CR1, immunoglobulin Gm and Km allotypes, FcγRIIA and FcγRIIIA (both Ig G Fc receptors), and heat shock protein 70.