The pathogenesis of systemic lupus erythematosus.
SLE is a complex, heterogeneous disease, the precise pathogenesis of which remains something of a mystery. In recent years our understanding has been advanced by the development of novel genetic and immunological techniques. Susceptibility to SLE has a genetic component and multiple putative genes are being investigated. The genes involved are likely to play a part in immune regulation. Central to the immune dysfunction seen in SLE is the presence of autoreactive B cells, which predominantly target nuclear antigens. In addition to evidence of aberrant B and T cell behaviour, lupus is associated with complement deficiencies, and abnormal cytokine function. A number of environmental triggers exist, and likely candidates include viral infection and exposure to UV light. Finally, evidence is accumulating that implicates apoptosis as a mechanism by which disease may be provoked and propagated.
Manson
J J
JJ
Centre for Rheumatology, University College London Hospitals, Arthur Stanley House, 40-50 Tottenham Street, London W1T 4NJ, United Kingdom.
Isenberg
D A
DA
D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000209:etiology* / Q000235:genetics / Q000276:immunology