Literature DB >> 15377341

In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades.

I Sánchez-Carpintero1, A España, B Pelacho, N López Moratalla, D S Rubenstein, L A Diaz, M J López-Zabalza.   

Abstract

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.

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Year:  2004        PMID: 15377341     DOI: 10.1111/j.1365-2133.2004.06147.x

Source DB:  PubMed          Journal:  Br J Dermatol        ISSN: 0007-0963            Impact factor:   9.302


  30 in total

Review 1.  Tyrosine kinases in inflammatory dermatologic disease.

Authors:  Ricardo T Paniagua; David F Fiorentino; Lorinda Chung; William H Robinson
Journal:  J Am Acad Dermatol       Date:  2010-06-26       Impact factor: 11.527

2.  Protective endogenous cyclic adenosine 5'-monophosphate signaling triggered by pemphigus autoantibodies.

Authors:  Volker Spindler; Franziska Vielmuth; Enno Schmidt; David S Rubenstein; Jens Waschke
Journal:  J Immunol       Date:  2010-10-29       Impact factor: 5.422

3.  Novel mechanisms of target cell death and survival and of therapeutic action of IVIg in Pemphigus.

Authors:  Juan Arredondo; Alexander I Chernyavsky; Ali Karaouni; Sergei A Grando
Journal:  Am J Pathol       Date:  2005-12       Impact factor: 4.307

4.  The extent of desmoglein 3 depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasal epidermal skin splitting?

Authors:  Volker Spindler; Alexander Endlich; Eva Hartlieb; Franziska Vielmuth; Enno Schmidt; Jens Waschke
Journal:  Am J Pathol       Date:  2011-08-22       Impact factor: 4.307

Review 5.  Cell adhesion in epidermal development and barrier formation.

Authors:  Kaelyn D Sumigray; Terry Lechler
Journal:  Curr Top Dev Biol       Date:  2015-02-11       Impact factor: 4.897

6.  Efficacy of intravenous immunoglobulin (IVIG) affinity-purified anti-desmoglein anti-idiotypic antibodies in the treatment of an experimental model of pemphigus vulgaris.

Authors:  D Mimouni; M Blank; A S Payne; G J Anhalt; C Avivi; I Barshack; M David; Y Shoenfeld
Journal:  Clin Exp Immunol       Date:  2010-10-21       Impact factor: 4.330

7.  Antimitochondrial autoantibodies in pemphigus vulgaris: a missing link in disease pathophysiology.

Authors:  Steve Marchenko; Alexander I Chernyavsky; Juan Arredondo; Vivian Gindi; Sergei A Grando
Journal:  J Biol Chem       Date:  2009-12-10       Impact factor: 5.157

8.  Desmosomes in vivo.

Authors:  David Garrod
Journal:  Dermatol Res Pract       Date:  2010-06-24

9.  Pemphigus vulgaris IgG-induced desmoglein-3 endocytosis and desmosomal disassembly are mediated by a clathrin- and dynamin-independent mechanism.

Authors:  Emmanuella Delva; Jean Marie Jennings; Cathárine C Calkins; Margaret D Kottke; Victor Faundez; Andrew P Kowalczyk
Journal:  J Biol Chem       Date:  2008-04-23       Impact factor: 5.157

10.  Disruption of desmosome assembly by monovalent human pemphigus vulgaris monoclonal antibodies.

Authors:  Xuming Mao; Eun Jung Choi; Aimee S Payne
Journal:  J Invest Dermatol       Date:  2008-11-27       Impact factor: 8.551

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