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Autoimmune Diseases
Volume 2013 (2013), Article ID 728529, 11 pages
Review Article

p38 MAPK Signaling in Pemphigus: Implications for Skin Autoimmunity

1Cellular Immunotherapy and Molecular Immunodiagnostics, Institute for Research and Technology-Thessaly (I.RE.TE.TH), 41222 Larissa, Greece
2Institute of Liver Studies, Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, Denmark Hill Campus, London SE5 9RS, UK
3Department of Animal Production, Technological Educational Institute of Larissa, 41110 Larissa, Greece
4Department of Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Viopolis, 41110 Larissa, Greece

Received 21 February 2013; Revised 18 June 2013; Accepted 19 June 2013

Academic Editor: Jozélio Freire De Carvalho

Copyright © 2013 Athanasios Mavropoulos 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.


p38 mitogen activated protein kinase (p38 MAPK) signaling plays a major role in the modulation of immune-mediated inflammatory responses and therefore has been linked with several autoimmune diseases. The extent of the involvement of p38 MAPK in the pathogenesis of autoimmune blistering diseases has started to emerge, but whether it pays a critical role is a matter of debate. The activity of p38 MAPK has been studied in great detail during the loss of keratinocyte cell-cell adhesions and the development of pemphigus vulgaris (PV) and pemphigus foliaceus (PF). These diseases are characterised by autoantibodies targeting desmogleins (Dsg). Whether autoantibody-antigen interactions can trigger signaling pathways (such as p38 MAPK) that are tightly linked to the secretion of inflammatory mediators which may perpetuate inflammation and tissue damage in pemphigus remains unclear. Yet, the ability of p38 MAPK inhibitors to block activation of the proapoptotic proteinase caspase-3 suggests that the induction of apoptosis may be a consequence of p38 MAPK activation during acantholysis in PV. This review discusses the current evidence for the role of p38 MAPK in the pathogenesis of pemphigus. We will also present data relating to the targeting of these cascades as a means of therapeutic intervention.