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: David S Rubenstein, Luis A Diaz (Affiliation: Department of Dermatology, University of North Carolina-Chapel Hill, Chapel Hill, NC 27599-7287, USA. druben at med.unc.edu)
• Journal: Autoimmunity (Autoimmunity) Vol. 39 Issue 7 Pg. 577-86 (Nov 2006) ISSN: 0891-6934 [Print] England
• PMID: 17101501 (Publication Type: Journal Article, Review)

Chemical References

• Autoantibodies
• Proteins

Topics

• Animals
• Autoantibodies (physiology)
• Humans
• Keratinocytes (immunology, metabolism)
• Pemphigus (immunology, metabolism, pathology)
• Phosphorylation
• Proteins (metabolism)