Pemphigus, a pathomechanism of acantholysis.
Australas J Dermatol
; 58(3): 171-173, 2017 Aug.
Article
em En
| MEDLINE
| ID: mdl-28211055
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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Autoanticorpos
/
Acantólise
/
Pênfigo
/
Proteínas Quinases p38 Ativadas por Mitógeno
/
Desmogleína 1
/
Desmogleína 3
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Australas J Dermatol
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Japão