Cutaneous Biology: In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades
Keywords: 
Calmodulin/antagonists & inhibitors/physiology
Immunoglobulin G/immunology
Protein Kinases/physiology
Issue Date: 
2004
Publisher: 
Wiley-Blackwell
ISSN: 
0007-0963
Citation: 
Sanchez-Carpintero I, Espana A, Pelacho B, Lopez Moratalla N, Rubenstein DS, Diaz LA, et al. In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades. Br J Dermatol 2004 Sep;151(3):565-570.
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 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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