Molecular insights into systemic lupus erythematosus pathogenesis.

Systemic lupus erythematosus (SLE) is a complex, heterogeneous, and chronic autoimmune disorder of an unknown origin. Its clinical symptoms range from a benign skin disorder to severe, life-threatening conditions.1 Immune effector dysfunctions are hall marks of SLE disease.2 The etiopathogenesis of the altered immune response in SLE remains unknown. SLE is characterized by the presence of auto-antibodies (AutoAbs) for a wide variety of self antigens and circulating immune complexes.1,2 The onset of lupus is variable and may affect all stages of life. The disease predominantly affiicts females in the child-bearing years about 6- to 10-fold more frequently than males. We have not had a new drug in 50 years, because of the unknown etiology of the abnormal immune response. The current lupus therapies are non-specific, symptomatic, and cause significant side effects. In this editorial, I have made an attempt to describe multistep immune alterations that pave the way for the inception and sustaining of SLE pathogenesis, and postulated molecular mechanisms involved in SLE disease onset. Such information will help in better understanding SLE etiopathogenesis and in developing effective and safer strategies to combat SLE as well as other autoimmune diseases.