Pemphigus, a pathomechanism of acantholysis

Masutaka Furue, Takafumi Kadono

研究成果: Contribution to journalReview article査読

6 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)171-173
ページ数3
ジャーナルAustralasian Journal of Dermatology
58
3
DOI
出版ステータス出版済み - 8 2017

All Science Journal Classification (ASJC) codes

  • Dermatology

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