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Basic and translational research
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Potential involvement of the IL-33–ST2 axis in the pathogenesis of primary Sjögren's syndrome
  1. Ahmad Awada1,2,
  2. Charles Nicaise3,4,
  3. Sabrina Ena5,
  4. Liliane Schandéné6,
  5. Joanne Rasschaert2,
  6. Iuliana Popescu7,
  7. Valérie Gangji1,2,
  8. Muhammad S Soyfoo1,2
  1. 1Department of Rheumatology and Physical Medicine, Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium
  2. 2Laboratory of Bone and Metabolic Biochemistry, Université Libre de Bruxelles, Brussels, Belgium
  3. 3Department of Pathology, Hôpital Erasme, Université libre de Bruxelles, Brussels, Belgium
  4. 4DIAPATH—Center for Microscopy and Molecular Imaging (CMMI), Gosselies, Belgium
  5. 5Laboratory of Neurophysiology, Université libre de Bruxelles, Brussels, Belgium
  6. 6Department of Immunobiology Clinic, Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium
  7. 7Laboratory of General Histology, Neuroanatomy and Neuropathology, Université Libre de Bruxelles, Brussels, Belgium
  1. Correspondence to Dr Muhammad S Soyfoo, Department of Rheumatology, Hôpital Erasme, Université libre de Bruxelles, 808 Route de Lennik, Brussels B-1070, Belgium; msoyfoo{at}ulb.ac.be

Abstract

Objectives To investigate the role of the interleukin (IL)-33–ST2 axis in the pathophysiology of primary Sjögren's syndrome (pSS).

Methods Serum levels of IL-33 and sST2 were determined by ELISA. The expression of IL-33 and ST2 was investigated in salivary glands (SG) by immunohistochemistry. PBMC were isolated and stimulated with IL-33, IL-12 and IL-23 and the cytokine profile response was examined by flow cytometry. Intracellular cytokine detection of IFNγ and IL-17 was performed by flow cytometry.

Results Serum IL-33 and sST2 levels were increased in pSS patients compared with controls and patients with systemic lupus erythematosus. Expression of IL-33 was upregulated in SG with Chisholm scores of 2 and 3 of pSS patients but comparable with controls for SG with Chisholm score of 4. ST2 expression in SG was downregulated in pSS patients. IL-33 at different concentrations did not increase the secretion of pro-inflammatory cytokines but acted synergistically with IL-12 and IL-23 to promote IFNγ production. NK and NKT cells were identified as main producers of IFNγ in vitro and were found in SG of pSS patients.

Conclusions IL-33 is released in pSS, and acts with IL-12 and IL-23 to favour the secretion of IFNγ by NK and NKT cells.

  • Sjögren's Syndrome
  • Cytokines
  • Autoimmunity
  • Inflammation

https://doi.org/10.1136/annrheumdis-2012-203187

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