p38 MAPK Signaling in Pemphigus: Implications for Skin Autoimmunity

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...

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Bibliographic Details
Published in:Autoimmune Diseases 2013-01, Vol.2013 (2013), p.158-168
Main Authors: Mavropoulos, Athanasios, Orfanidou, Timoklia, Liaskos, Christos, Smyk, Daniel S., Spyrou, Vassiliki, Sakkas, Lazaros I., Rigopoulou, Eirini I., Bogdanos, Dimitrios P.
Format: Article
Language:English
Subjects:
Adhesion
Antibodies
Apoptosis
Autoantibodies
Autoimmune diseases
Caspase-3
Cellular signal transduction
Chemokines
Cytokines
Flow cytometry
Gene expression
Histopathology
Inflammation
Kinases
MAP kinase
Mitogen-activated protein kinases
Pathogenesis
Pathology
Pemphigus
Phosphorylation
Physiological aspects
Physiological research
Properties
Protein kinase
Proteinase
Proteins
Psoriasis
Review
Signal transduction
Skin
Tumor necrosis factor-TNF
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Summary: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.
ISSN:2090-0430
2090-0422
2090-0430
DOI:10.1155/2013/728529