title: Pemphigus antibody induced phosphorylation of keratinocyte proteins.
abstract: 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.
authors.affiliation: Department of Dermatology, University of North Carolina-Chapel Hill, Chapel Hill, NC 27599-7287, USA. druben@med.unc.edu
authors.forename: David S
authors.initials: DS
authors.lastname: Rubenstein
authors.forename: Luis A
authors.initials: LA
authors.lastname: Diaz
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000502:physiology*; D006801:Humans; D015603:Keratinocytes / Q000276:immunology / Q000378:metabolism*; D010392:Pemphigus / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D011506:Proteins / Q000378:metabolism*
chemical_list: D001323:Autoantibodies; D011506:Proteins