Effects of interleukin-34 on CCL28 expression of fibroblast-like synoviocytes in rheumatoid arthritis patients
10.3969/j.issn.1000-484X.2018.02.016
- VernacularTitle:白细胞介素-34对类风湿关节炎成纤维样滑膜细胞CCL28表达的影响
- Author:
Xun-Li OUYANG
1
;
Han LI
;
Xiao-Tong SUN
;
Yan ZHANG
;
Xia LI
;
Jing WEI
Author Information
1. 大连医科大学
- Keywords:
Rheumatoid arthritis;
Interleukin-34;
Fibroblast-like synoviocytes;
CC chemokine ligand 28
- From:
Chinese Journal of Immunology
2018;34(2):239-242
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of interleukin-34(IL-34)on the expression of CC chemokine ligand 28 (CCL28) by fibroblast-like synoviocytes(FLS) in rheumatoid arthritis(RA) patients.Methods:FLS were isolated from 6 RA patients and stimulated with IL-34,IL-34 receptor antagonist /IL-34,inhibitors of signaling pathway/IL-34 in vitro respectively.CCL28 mRNA expression was measured by reverse transcription polymerase chain reaction(RT-PCR).The level of CCL28 in the supernatant of RA FLS culture was detected by enzyme linked immunosorbent assay(ELISA).Statistical analysis between groups was performed by t test.Results:Compared with unstimulated FLS,CCL28 expression was increased obviously in IL-34-stimulated group(P<0.05).The level of CCL28 was significantly decreased when anti-IL-34 antibody was added into IL-34-administrated RA FLS(P<0.05).While after adding of nuclear factor κB(NF-κB) and mitogen-activated protein kinase38(p38 MAPK) signaling pathway inhibitors into the cell culture system,CCL28 expression was remarkably reduced (P<0.05).Conclusion: The secretion of CCL28 by RA FLS can be promoted by the binding of IL-34 with its specific receptor via the activation of NF-κB and p38 MAPK signaling pathways,which suggests that CCL28 might be involved in the pathogenesis of RA.
