• Lazaros I Sakkas and Dimitrios P Bogdanos.
• Department of Rheumatology and Clinical Immunology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece. Electronic address: lsakkas@med.uth.gr.
• Autoimmun Rev. 2017 Jan 1; 16 (1): 10-15.

AbstractPsoriatic arthritis (PsA) is a psoriasis (Ps)-associated inflammatory joint disease that affects peripheral joints, entheses, spine, and eyes. PsA and Ps are likely to be the same disease. PsA develops in nearly 70% of patients with Ps, and the hallmark of the disease is bone erosions and bone formation. Both innate and adaptive immunity appear to contribute to pathogenesis of PsA and Ps. Trauma may be a trigger factor for both PsA and Ps. The same T cell clones were reported to be present in both synovial tissues and skin lesions suggesting that a common antigen drives T cell immune response in the joints and skin lesions of patients with PsA. The IL-23/IL-17 axis plays a critical pathogenic role for both PsA and Ps, and biologics neutralizing IL-17A or IL-23/IL-12 are effective therapies for PsA and Ps. The differential expression of Th17 cytokines IL-17 and IL-22 at various sites could explain the different manifestations of the disease. IL-17 is highly expressed in peripheral joints and skin lesions and causes bone erosions. IL-22 is highly expressed in skin lesions and entheses, not peripheral joints, and cause bone formation. Finally, mannan from baker's yeast caused PsA-like arthritis and Ps-like skin lesions that were blocked by IL-17 treatment. These data suggest that PsA and Ps are likely to be the same disease exhibiting different manifestations depending on the local cytokine production.Copyright © 2016 Elsevier B.V. All rights reserved.

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