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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
Kelly N. MESSINGHAM 1, Grant RANDALL 1, Janet FAIRLEY 1, 2
1 Veterans Administration Medical Center, Iowa City, IA, USA; 2 Department of Dermatology, University of Iowa, Iowa City, IA, USA
Bullous pemphigoid (BP) is the most common autoimmune blistering disease characterized by pathogenic autoantibodies targeting collagen XVII (col XVII), a hemidesmosomal adhesion molecule. Early studies utilizing IgG were critical for establishing col XVII-specific antibodies as primary mediators of blister formation; however, these studies lacked key features of the disease, including urticarial erythema and eosinophilic infiltration, which are often associated with IgE. Although it was recognized that BP patients often had elevated circulating IgE, investigations into the pathogenicity of these antibodies was delayed until discovery of col XVII-specific IgE in BP sera. Since then, a variety of in-vivo and in-vitro studies have provided clear evidence that IgE autoantibodies are a key component of BP. Furthermore, studies utilizing IgE receptor blockade in BP patients were the first to confirm a pathogenic role of IgE autoantibodies in human autoimmunity. In this review we will utilize BP as a prototypical autoimmune disease to better understand how IgE autoantibodies participate in human autoimmunity.