Scientific publications

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

Sep 1, 2004 | Magazine: The British Journal of Dermatology

Sánchez-Carpintero I, España A, Pelacho B, López Moratalla N, Rubenstein DS, Diaz LA, López-Zabalza MJ.

Pemphigus vulgaris (PV) is an autoimmune disease characterized by mucocutaneous intraepithelial blisters and pathogenic autoantibodies against desmoglein. The mechanism of blister formation in pemphigus has not been defined; however, in vitro data suggest a role for activation of intracellular signalling cascades.

To investigate the contribution of these signalling pathways to the mechanism of PV IgG-induced acantholysis in 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 acantholysis in vivo.

These observations strongly support the role of intracellular signalling cascades in the molecular mechanism of PV IgG-induced acantholysis.

CITATION Br J Dermatol. 2004 Sep;151(3):565-70

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