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Open Access Highly Accessed Research article

Th17 and Th22 cells in psoriatic arthritis and psoriasis

Helen Benham13*, Paul Norris2, Jane Goodall3, Mihir D Wechalekar45, Oliver FitzGerald6, Agnes Szentpetery6, Malcolm Smith45, Ranjeny Thomas1 and Hill Gaston3

Author Affiliations

1 The University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba QLD 4102, Australia

2 Department of Dermatology Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0QQ, UK

3 Department of Medicine, University of Cambridge, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0QQ, UK

4 Rheumatology Unit, Repatriation General Hospital, 216 Daws Rd, Daw Park, South Australia 5042, Australia

5 Flinders University, Bedford Park, Sturt Rd, South Australia 5042, Australia

6 Department of Rheumatology, St Vincent’s University Hospital, Merrion Rd, Dublin 4, and The Conway Institute for Biomolecular Research, University College Dublin, Belfield, Dublin 4, Dublin, Ireland

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Arthritis Research & Therapy 2013, 15:R136  doi:10.1186/ar4317

Published: 26 September 2013

Abstract

Introduction

The aim of this study was to characterize interleukin 17 (IL-17) and interleukin 22 (IL-22) producing cells in peripheral blood (PB), skin, synovial fluid (SF) and synovial tissue (ST) in patients with psoriasis (Ps) and psoriatic arthritis (PsA).

Methods

Flow cytometry was used to enumerate cells making IL-22 and IL-17, in skin and/or SF and PB from 11 patients with Ps and 12 patients with PsA; skin and PB of 15 healthy controls and SF from rheumatoid arthritis (RA) patients were used as controls. Expression of the interleukin 23 receptor (IL-23R) and chemokine receptors CCR4 and CCR6 was examined. Secretion of IL-17 and IL-22 was measured by ELISA. ST was analysed by immunohistochemical staining of IL-17 and IL-22.

Results

Increased frequencies of IL-17+ and IL-22+ CD4+ T cells were seen in PB of patients with PsA and Ps. IL-17 secretion was significantly elevated in both PsA and Ps, whilst IL-22 secretion was higher in PsA compared to Ps and healthy controls. A higher proportion of the CD4+ cells making IL-17 or IL-22 expressed IL-23R and frequencies of IL-17+, CCR6+ and CCR4+ T cells were elevated in patients with Ps and those with PsA. In patients with PsA, CCR6+ and IL-23R + T cells numbers were elevated in SF compared to PB. Increased frequencies of IL-17+ and IL-22+ CD4+ T cells were demonstrated in Ps skin lesions. In contrast, whilst elevated frequencies of CD4+ IL-17+ cells were seen in PsA SF compared to PB, frequencies of CD4+ IL-22+ T cells were lower. Whereas IL-17 expression was equivalent in PsA, osteoarthritis (OA) and RA ST, IL-22 expression was higher in RA than either OA or PsA ST, in which IL-22 was strikingly absent.

Conclusions

Elevated frequencies of IL-17 and IL-22 producing CD4+ T cells were a feature of both Ps and PsA. However their differing distribution at disease sites, including lower frequencies of IL-22+ CD4+ T cells in SF compared to skin and PB, and lack of IL-22 expression in ST suggests that Th17 and Th22 cells have common, as well as divergent roles in the pathogenesis of Ps and PsA.