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In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades
Author(s) -
SánchezCarpintero I.,
España A.,
Pelacho B.,
López Moratalla N.,
Rubenstein D.S.,
Diaz L.A.,
LópezZabalza M.J.
Publication year - 2004
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2004.06147.x
Subject(s) - acantholysis , medicine , library science , dermatology , computer science , immunology , autoantibody , antibody
Summary Background 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 vitro data suggest a role for activation of intracellular signalling cascades. Objectives To investigate the contribution of these signalling pathways to the mechanism of PV IgG‐induced acantholysis in vivo . Methods 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. Results Inhibitors of tyrosine kinases, phospholipase C, calmodulin and the serine/threonine kinase protein kinase C prevented PV IgG‐induced acantholysis in vivo . Conclusions These observations strongly support the role of intracellular signalling cascades in the molecular mechanism of PV IgG‐induced acantholysis.