Novel mechanism for therapeutic action of IVIg in autoimmune blistering dermatoses.

Abstract

The mode of action of intravenous immunoglobulin (IVIg) is complex. An ongoing research continues to elaborate and identify novel mechanisms. Recent advances have demonstrated that IVIg has direct effect on keratinocytes, the target cells of autoimmune blistering diseases. IVIg protects keratinocytes from pathogenic autoantibodies by preventing the autoantibody-induced of apoptosis and oncosis. This anti-apoptotic action of IVIg helps explain how IVIg works in severe, life threatening dermatologic conditions that are resistant to traditional systemic treatments, such as toxic epidermal necrolysis and Stevens-Johnson syndrome. Thus, the actions of IVIg are varied and complex, and the primary mechanisms of action may be different in different diseases.