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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 569751, 8 pages
Review Article

The Role of p38 MAPK in the Aetiopathogenesis of Psoriasis and Psoriatic Arthritis

1Cellular Immunotherapy and Molecular Immunodiagnostics, Institute of Research and Technology Thessaly, 41222 Larissa, Greece
2Division of Transplantation Immunology and Mucosal Biology, Institute of Liver Studies, King’s College London School of Medicine at King’s College Hospital, Denmark Hill Campus, London SE5 9RS, UK
3Department of Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Biopolis, 41110 Larissa, Greece
4Center of Molecular Medicine, Old Dominion University, 23529 Monarch Way, Norfolk, VA, USA
5Department of Rheumatology, Faculty of Medicine School of Health Sciences, University of Thessaly, Biopolis, 41110 Larissa, Greece

Received 5 July 2013; Accepted 14 August 2013

Academic Editor: Yehuda Shoenfeld

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.


The pathogenetic mechanisms responsible for the induction of immune-mediated disorders, such as psoriasis, remain not well characterized. Molecular signaling pathways are not well described in psoriasis, as well as psoriatic arthritis, which is seen in up to 40% of patients with psoriasis. Signaling pathway defects have long been hypothesized to participate in the pathology of psoriasis, yet their implication in the altered psoriatic gene expression still remains unclear. Emerging data suggest a potential pathogenic role for mitogen activated protein kinases p38 (p38 MAPK) extracellular signal-regulated kinase 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) in the development of psoriasis. The data are still limited, though, for psoriatic arthritis. This review discusses the current data suggesting a crucial role for p38 MAPK in the pathogenesis of these disorders.