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Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjögren's syndrome
  1. Francesco Ciccia1,
  2. Giuliana Guggino1,2,
  3. Aroldo Rizzo3,
  4. Angelo Ferrante1,
  5. Stefania Raimondo2,
  6. AnnaRita Giardina1,
  7. Francesco Dieli2,
  8. Giuseppina Campisi4,
  9. Riccardo Alessandro2,
  10. Giovanni Triolo1
  1. 1Dipartimento Biomedico di Medicina Interna e Specialistiche, Sezione di Reumatologia, Università di Palermo, Palermo, Italy
  2. 2Dipartimento di Biopatologia e Biotecnologie Mediche e Forensi, Università di Palermo, Palermo, Italy
  3. 3Azienda Ospedaliera Ospedali Riuniti Villa Sofia-Cervello, Anatomia Patologica, Palermo, Italy
  4. 4Dipartimento di Discipline Chirurgiche ed Oncologiche, Università degli Studi di Palermo, Palermo, Italy
  1. Correspondence to Professor Giovanni Triolo, Dipartimento Biomedico di Medicina Interna e Specialistiche, Sezione di Reumatologia, Istituto di Clinica Medica, Università di Palermo, Palermo 90127, Italy; giovanni.triolo{at}unipa.it

Abstract

Objectives In chronic inflammatory disorders, interleukin (IL)-22 may act either as a protective or as a pro-inflammatory cytokine. At mucosal sites, IL-22 is mainly produced by CD4+ T cells and by a subset of mucosal natural killer (NK) cells expressing the receptor NKp44 (NKp44+ NK cells). The aim of this study was to investigate the IL-22 expression in the salivary glands of patients with primary Sjögren's syndrome (pSS).

Methods Minor salivary gland biopsies were obtained from 19 patients with pSS and 16 with non-specific chronic sialoadenitis. Quantitative gene expression analysis by TaqMan real-time PCR and immunohistochemistry for IL-17, IL-22, IL-23 and STAT3 (signal transducer and activator of transcription) was performed on salivary glands from patients and controls. The cellular sources of IL-22 among infiltrating inflammatory cells were also determined by fluorescence-activated cell sorting analysis and immunohistochemistry.

Results IL-22, IL-23 and IL-17 were significantly increased at both protein and mRNA levels in the inflamed salivary glands of patients with pSS. STAT3 mRNA and the tyrosine phosphorylated corresponding protein were also significantly increased in pSS. Th17 and NKp44+ NK cells were the major cellular sources of IL-22 in patients with pSS.

Conclusions Our results suggest that, together with IL-17 and IL-23, IL-22 may play a pro-inflammatory role in the pathogenesis of pSS.

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Footnotes

  • FC and GG contributed equally to this work. RA and GT shared co-senior authorship.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the University of Palermo.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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