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Dermatology Research and Practice
Volume 2010, Article ID 456841, 8 pages
http://dx.doi.org/10.1155/2010/456841
Review Article

Apoptotic Pathways in Pemphigus

1Department of Dermatology, University of North Carolina-Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA
2Department of Pharmacology, University of North Carolina-Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA
3Lineberger Comprehensive Cancer Center, University of North Carolina-Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA

Received 14 December 2009; Accepted 24 February 2010

Academic Editor: Mỹ G. Mahoney

Copyright © 2010 Meryem Bektas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Pemphigus is a group of human autoimmune blistering diseases of the skin in which autoantibodies to desmosome cadherins induce loss of cell-cell adhesion (acantholysis). In addition to steric hindrance and activation of intracellular signaling, apoptosis has been suggested to contribute to the mechanism by which pathogenic IgG induces acantholysis. We review the current literature examining the role of apoptosis in pemphigus. Current data suggest that apoptosis is not required for blister induction, but that activation of proapoptotic proteins, including caspase cysteine proteinases, may sensitize cells to the acantholytic effects of pemphigus IgG.