Epidermolysis bullosa acquisita: From pathophysiology to novel therapeutic options

Michael Kasperkiewicz, Christian D. Sadik, Katja Bieber, Saleh M. Ibrahim, Rudolf A. Manz, Enno Schmidt, Detlef Zillikens, Ralf J. Ludwig

Research output: Contribution to journalReview articlepeer-review

80 Scopus citations

Abstract

Epidermolysis bullosa acquisita (EBA) is a prototypic organ-specific autoimmune disease induced by autoantibodies to type VII collagen causing muco-cutaneous blisters. In the inflammatory (bullous pemphigoid-like) EBA variant, autoantibody binding is followed by a lesional inflammatory cell infiltration, and the overall clinical picture may be indistinguishable from that of bullous pemphigoid, the latter being the most common autoimmune bullous disease. The last decade witnessed the development of several mouse models of inflammatory EBA that facilitated the elucidation of the pathogenesis of autoantibody-induced, cell-mediated subepidermal blistering diseases and identified new therapeutic targets for these and possibly other autoantibody-driven disorders.

Original languageBritish English
Pages (from-to)24-33
Number of pages10
JournalJournal of Investigative Dermatology
Volume136
Issue number1
DOIs
StatePublished - Jan 2016

Fingerprint

Dive into the research topics of 'Epidermolysis bullosa acquisita: From pathophysiology to novel therapeutic options'. Together they form a unique fingerprint.

Cite this