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.