Background/Purpose: To determine the involvement of S100A8/A9 in the pathogenesis of primary Sjögren’s syndrome (pSS)

Methods:

The serum levels of S100A8/A9, IL-17A and IL-17C were determined by ELISA. The expression of S100A8/A9, TLR4, IL-17A, IL-17C, IL-17RA, IL-17RC and IL-17RE was assessed by immunohistochemistry. PBMCs were isolated from 10 pSS patients and 10 healthy controls, stimulated with increasing concentrations of S100A8/A9 and interferon-γ. The cytokine profile was next investigated by flow cytometry and ELISA.

Results: Serum levels of S100A8/A9 were increased in pSS patients compared to controls. The expressions of S100A8/A9, TLR4, IL-17A, IL-17C, IL-17RA, IL-17RC, IL-17RE were enhanced in the salivary glands of pSS patients. No significant serum levels of IL-17A and IL-17C were detected in both groups of patients. S100A8/A9 significantly increased the production of TNF-α and IL-1β in pSS patients. We observed increased production of IL-17A following stimulation with S100A8/A9 but not achieving statistical significance. No secretion of IL-17C was detected upon PBMC’s stimulation by S100A8/A9. Moreover, S100A8/A9 with IFN-γ synergistically increased significantly the production of TNF-α and IL-1β.

Conclusion: S100A8/A9 is increased in pSS and contributed to the increased production of TNF-α and IL-1β alone and in synergy with IFN-γ. S100A8/A9 induced the secretion of IL-17A in controls and pSS patients. IL-17A, IL-17C and their respective receptors were upregulated in the salivary glands of pSS patients.

ACR Meeting Abstracts - https://acrabstracts.org/abstract/s100a8a9-is-upregulated-and-triggers-the-secretion-of-pro-inflammatory-cytokines-in-primary-sjogrens-syndrome/