| Literature DB >> 29037765 |
Volker Spindler1, Rüdiger Eming2, Enno Schmidt3, Masayuki Amagai4, Sergei Grando5, Marcel F Jonkman6, Andrew P Kowalczyk7, Eliane J Müller8, Aimee S Payne9, Carlo Pincelli10, Animesh A Sinha11, Eli Sprecher12, Detlef Zillikens13, Michael Hertl2, Jens Waschke14.
Abstract
The autoimmune blistering skin disease pemphigus is caused by IgG autoantibodies against desmosomal cadherins, but the precise mechanisms are in part a matter of controversial discussions. This review focuses on the currently existing models of the disease and highlights the relevance of desmoglein-specific versus nondesmoglein autoantibodies, the contribution of nonautoantibody factors, and the mechanisms leading to cell dissociation and blister formation in response to autoantibody binding. As the review brings together the majority of laboratories currently working on pemphigus pathogenesis, it aims to serve as a solid basis for further investigations for the entire field.Entities:
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Year: 2017 PMID: 29037765 DOI: 10.1016/j.jid.2017.06.022
Source DB: PubMed Journal: J Invest Dermatol ISSN: 0022-202X Impact factor: 8.551