Pemphigus antibody induced phosphorylation of keratinocyte proteins.

The pemphigus family of autoimmune blistering diseases is characterized by an autoantibody response to desmosomal cadherins in epithelia. Autoantibodies against desmogleins, desmosome cell adhesion molecules, induce loss of cell-cell adhesion that is characterized clinically by blister formation. The mechanism by which these autoantibodies induce loss of cell-cell adhesion is under active investigation, but appears to involve a coordinated intracellular response including activation of intracellular signaling and phosphorylation of a number of proteins in the target keratinocyte. Activation of p38 mitogen activated protein kinase may have a critical role in the acantholytic mechanism as inhibitors of p38MAPK block the ability of pemphigus IgG to induce blistering in pemphigus animal models.