Complement-independent blistering mechanisms in bullous pemphigoid
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Updated: Aug 17, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Hiroaki Iwata1, Hideyuki Ujiie1
1Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Abstract:
Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease that clinically demonstrates tense blisters with widespread erythema, histologically demonstrates subepidermal blistering and immunologically demonstrates the presence of circulating autoantibodies against hemidesmosomal molecules. Complement activation has long been regarded as necessary for the generation of the BP. However, certain evidence has recently come to support non-complemental blistering mechanisms. The story of BP blistering mechanisms is a complicated one. This review mainly focuses on a specific blistering mechanism that highlights the role of complements in BP blistering.
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