Pemphigus, a pathomechanism of acantholysis

Masutaka Furue, Takafumi Kadono

Research output: Contribution to journalReview article

6 Citations (Scopus)

Abstract

Autoantibodies to the desmosomal proteins desmoglein 1 and 3 cause pemphigus foliaceus and pemphigus vulgaris, which are characterised by keratinocyte dissociation (acantholysis) and intraepidermal blister formation. The passive transfer of pathogenic anti-desmoglein antibodies induces blisters in mice in vivo and the loss of keratinocyte adhesion in vitro. The pathogenetic mechanisms of acantholysis due to anti-desmoglein autoantibodies are not fully understood. However, recent studies have revealed that signalling-dependent and signalling-independent pathways are operative in the loss of cell adhesion. In this review, we focus on the pathomechanism of acantholysis due to autoantibodies to desmogleins and recent therapeutic approaches.

Original languageEnglish
Pages (from-to)171-173
Number of pages3
JournalAustralasian Journal of Dermatology
Volume58
Issue number3
DOIs
Publication statusPublished - Aug 2017

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All Science Journal Classification (ASJC) codes

  • Dermatology

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