학술논문
In vivoblockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades.
Document Type
Article
Author
Source
Subject
*AUTOIMMUNE diseases
*BLISTERS
*PEMPHIGUS
*AUTOANTIBODIES
*LABORATORY mice
*IMMUNOGLOBULIN G
*SKIN diseases
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Language
ISSN
0007-0963
Abstract
Pemphigus vulgaris (PV) is an autoimmune disease characterized by mucocutaneous intraepithelial blisters and pathogenic autoantibodies against desmoglein 3. The mechanism of blister formation in pemphigus has not been defined; however,in vitrodata suggest a role for activation of intracellular signalling cascades.To investigate the contribution of these signalling pathways to the mechanism of PV IgG-induced acantholysisin vivo.We used the passive transfer mouse model. Mice were injected with IgG fractions of sera from a patient with PV, with or without pretreatment with inhibitors of proteins that mediate intracellular signalling cascades.Inhibitors of tyrosine kinases, phospholipase C, calmodulin and the serine/threonine kinase protein kinase C prevented PV IgG-induced acantholysisin vivo.These observations strongly support the role of intracellular signalling cascades in the molecular mechanism of PV IgG-induced acantholysis. [ABSTRACT FROM AUTHOR]