A diverse array of genetic factors contribute to the pathogenesis of Systemic Lupus Erythematosus
Abstract
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease with variable clinical presentation
frequently affecting the skin, joints, haemopoietic system, kidneys, lungs and central nervous system. It can be life
threatening when major organs are involved. The full pathological and genetic mechanisms of this complex disease
are yet to be elucidated; although roles have been described for environmental triggers such as sunlight, drugs and
chemicals, and infectious agents. Cellular processes such as inefficient clearing of apoptotic DNA fragments and
generation of autoantibodies have been implicated in disease progression. A diverse array of disease-associated
genes and microRNA regulatory molecules that are dysregulated through polymorphism and copy number
variation have also been identified; and an effect of ethnicity on susceptibility has been described.