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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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P38 MAPK signaling in pemphigus: Implications for skin autoimmunity

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Author
Mavropoulos, A.; Orfanidou, T.; Liaskos, C.; Smyk, D. S.; Spyrou, V.; Sakkas, L. I.; Rigopoulou, E. I.; Bogdanos, D. P.
Date
2013
DOI
10.1155/2013/728529
Keyword
adalimumab
autoantibody
caspase 3
cyclophosphamide
desmoglein
etanercept
glucocorticoid
infliximab
kc 706
methotrexate
mitogen activated protein kinase p38
mitogen activated protein kinase p38 inhibitor
mycophenolic acid 2 morpholinoethyl ester
rituximab
unclassified drug
apoptosis
autoimmunity
cell adhesion
corticosteroid therapy
drug withdrawal
enzyme activation
enzyme activity
enzyme inhibition
human
immunopathogenesis
immunosuppressive treatment
inflammation
keratinocyte
mediator
multicenter study (topic)
pemphigus
pemphigus foliaceus
pemphigus vulgaris
phase 2 clinical trial (topic)
priority journal
review
signal transduction
unspecified side effect
Metadata display
Abstract
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. © 2013 Athanasios Mavropoulos et al.
URI
http://hdl.handle.net/11615/30841
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19705]
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