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Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis

Authors
Hong, Yeon-SikMoon, Su-JinJoo, Young-BinJeon, Chan-HongCho, Mi-LaJu, Ji HyeonOh, Hye-JwaHeo, Yu-JungPark, Sung-HwanKim, Ho-YounMin, Jun-Ki
Issue Date
Sep-2011
Publisher
대한의학회
Keywords
Interleukin-33; sST2; ST2L; Arthritis; Rheumatoid
Citation
Journal of Korean Medical Science, v.26, no.9, pp 1132 - 1139
Pages
8
Journal Title
Journal of Korean Medical Science
Volume
26
Number
9
Start Page
1132
End Page
1139
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/16269
DOI
10.3346/jkms.2011.26.9.1132
ISSN
1011-8934
1598-6357
Abstract
The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 +/- 464.0 pg/mL) than in healthy controls (96.0 +/- 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1 beta (r= 0.311, P = 0.005), and IL-33 and IL-6 (r= 0.264, P= 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naive RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.
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