Sonali J. Bracken, Soman Abraham and Amanda S. MacLeod
Different theories exist to describe the pathogenesis of chronic spontaneous urticaria. A group of investigators highlighted in this study the evidence surrounding the autoimmune pathogenesis of chronic urticaria, a condition which persists for more than 6 weeks in duration and occurs in the absence of an identifiable provoking factor.
Chronic spontaneous urticaria results from pathogenic activation of mast cells and basophils, which releases proinflammatory mediators of urticaria. Recent data suggests that chronic spontaneous urticaria may involve contributions from both immunoglobin G (IgG)-specific and immunoglobulin E (IgE)-specific autoantibodies against a vast array of antigens that can span beyond those found on the surface of mast cells and basophils, contributing to the severity of the disease and predisposing people to the development of additional autoimmune diseases.
People with chronic spontaneous urticaria mediated by IgE autoantibodies appear to have a faster onset of improvement in response to omalizumab than those with IgG-mediated disease.