Increased Expression Of Interleukin 33 In Sera and Salivary Gland From Patients With Sjögren Syndrome

Seung Min Jung¹, Young Sun Suh², Jung Hee Koh², Jae Ho Lee², Jennifer Lee², Soo Young Lee³, Ji Hyeon Ju², Kyung-Su Park², Dae Chul Jeong⁴, Sung Hwan Park² and Seung-Ki Kwok¹, ¹Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea, ²Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, South Korea, ³Department of Pediatrics, School of Medicine, The Catholic University of Korea, Incheon St. Mary's Hospital, Incheon, South Korea, ⁴Division of Rheumatology, Department of Pediatrics, School of Medicine, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, South Korea

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Sjogren's syndrome and cytokines

Session Information

Title: Sjögren's Syndrome: Pathogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose: Interleukin 33 (IL-33), a member of IL-1 superfamily, exerts pro-inflammatory effect by binding with ST2 expressed on many cell types. Recently, the association of IL-33 with autoimmune disease has been increasingly reported. The aim of this study is to identify the expression of IL-33 and ST2 in sera and salivary gland tissues from patients with Sjögren syndrome (SS).

Methods: Serum level of IL-33 and expression of IL-33 in salivary gland were assessed in patients with and without SS by ELISA and immunohistochemistry, respectively. Difference in expression of ST2 between patients with and without SS was compared by mRNA level and ST2 positive cells in peripheral blood mononuclear cell (PBMC) from each group. The source of IL-33 in salivary gland of patients with SS was investigated using confocal microscopy system after staining with cytokeratin antibody, CD31 antibody and IL-33 antibody. Additionally, we examined mRNA expression of IL-33 from salivary gland cell line (human head and neck squamous cell carcinoma A253 cell) after stimulation with pro-inflammatory cytokines.

Results: Serum IL-33 level was significantly higher in SS group than that of control group (p=0.004). Immunohistochemistry of salivary gland also revealed increased expression of IL-33 in SS group. However, the level of ST2 mRNA in PBMC was lower in SS group than control group, although statistically not significant (p=0.093). Consistently, the proportion of ST2 positive cells in PBMC was smaller in SS patients (p=0.004). We demonstrated the expression of IL-33 in epithelial and endothelial cells from salivary gland of patients with SS. The expression of IL-33 mRNA in A253 cell was considerably increased after stimulation with interferon gamma.

Conclusion: Our result shows that IL-33 is involved in the pathogenesis of SS. Further research would suggest a new therapeutic approach associated with IL-33/ST2 pathway in SS.

Disclosure:

S. M. Jung,
None;

Y. S. Suh,
None;

J. H. Koh,
None;

J. H. Lee,
None;

J. Lee,
None;

S. Y. Lee,
None;

J. H. Ju,
None;

K. S. Park,
None;

D. C. Jeong,
None;

S. H. Park,
None;

S. K. Kwok,
None.

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