Background/Purpose: To investigate the role of IL-33/ST2 in the pathophysiology of primary Sjögren’s syndrome (pSS)
Methods: Serum levels of IL-33 and sST2 was determined by ELISA. The expression of IL-33 and ST2 was examined in the salivary glands of patients by immunohistochemistry and western blot. 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 IFN-gamma and IL-17 was performed by flow cytometry. RT-PCR was performed to detect IL-33, sST2 and ST2L transcripts after PBMC stimulation by TNF-a and IL-1b with and without LPS.
Results: IL-33 and sST2 was increased in pSS patients compared to controls. Expression of IL-33 was upregulated in the salivary glands of pSS patients with Chisholm scores of 2 and 3 but comparable to controls for patients with Chisholm score of 4. sST2 expression was downregulated in pSS patients. IL-33 in a dose related fashion increased the secretion of TNF, IL-1,IL-6 and IL-10. Moreover, IL-33 acts synergistically with IL-12 and IL-23 promoting IFN production. NK and NKT cells were identified as main producers of IFN. TNF and IL-1 increased the ST2L transcripts levels while no IL-33 expression was detected
Conclusion: IL-33 is released in pSS, favouring the secretion of pro-inflammatory cytokines.Our study reveals IL-33/ST2 axis in the pathophysiology of pSS.
Disclosure:
A. Awada,
None;
V. Gangji,
None;
M. S. Soyfoo,
None.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/involvement-of-interleukin-33-in-the-pathogenesis-of-sjogrens-syndrome/