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J Invest Dermatol. 2018 Jan;138(1):32-37. doi: 10.1016/j.jid.2017.06.022. Epub 2017 Oct 14.

Mechanisms Causing Loss of Keratinocyte Cohesion in Pemphigus.

Author information

1
Institute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität, Munich, Germany. Electronic address: volker.spindler@med.uni-muenchen.de.
2
Department of Dermatology, University of Marburg, Marburg, Germany.
3
Department of Dermatology, University of Lübeck, Lübeck, Germany; Lübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
4
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan.
5
Institute for Immunology and Departments of Dermatology and Biological Chemistry, University of California, Irvine, California, USA.
6
Department of Dermatology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
7
Departments of Cell Biology and Dermatology, Emory University, Atlanta, Georgia, USA.
8
Vetsuisse Faculty, Molecular Dermatology and Stem Cell Research, Institute of Animal Pathology, Bern, Switzerland; Vetsuisse Faculty, DermFocus, Bern, Switzerland; Department of Dermatology, University Hospital of Bern, Bern, Switzerland.
9
Department of Dermatology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
10
Laboratory of Cutaneous Biology, University of Modena and Reggio Emilia, Modena, Italy.
11
Department of Dermatology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA.
12
Department of Dermatology, Tel Aviv Medical Center, Tel Aviv, Israel.
13
Department of Dermatology, University of Lübeck, Lübeck, Germany.
14
Institute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität, Munich, Germany. Electronic address: jens.waschke@med.uni-muenchen.de.

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.

PMID:
29037765
DOI:
10.1016/j.jid.2017.06.022
[Indexed for MEDLINE]
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