Journal
BRITISH JOURNAL OF DERMATOLOGY
Volume 151, Issue 3, Pages 565-570Publisher
WILEY
DOI: 10.1111/j.1365-2133.2004.06147.x
Keywords
calmodulin; pemphigus vulgaris; phospholipase C; protein kinase C; tyrosine kinases
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Funding
- NIAID NIH HHS [R01 AI49427] Funding Source: Medline
- NIAMS NIH HHS [R01 AR32599, R01 AR32081, R01 AR032081] Funding Source: Medline
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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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