Pemphigus, a pathomechanism of acantholysis

Masutaka Furue, Takafumi Kadono

研究成果: ジャーナルへの寄稿評論記事

6 引用 (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.

元の言語英語
ページ(範囲)171-173
ページ数3
ジャーナルAustralasian Journal of Dermatology
58
発行部数3
DOI
出版物ステータス出版済み - 8 1 2017

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Desmogleins
Acantholysis
Pemphigus
Autoantibodies
Blister
Keratinocytes
Desmoglein 3
Desmoglein 1
Cell Adhesion
Anti-Idiotypic Antibodies
Proteins
Therapeutics

All Science Journal Classification (ASJC) codes

  • Dermatology

これを引用

Pemphigus, a pathomechanism of acantholysis. / Furue, Masutaka; Kadono, Takafumi.

:: Australasian Journal of Dermatology, 巻 58, 番号 3, 01.08.2017, p. 171-173.

研究成果: ジャーナルへの寄稿評論記事

Furue, Masutaka ; Kadono, Takafumi. / Pemphigus, a pathomechanism of acantholysis. :: Australasian Journal of Dermatology. 2017 ; 巻 58, 番号 3. pp. 171-173.
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