Immune Netw.
2007 Mar;7(1):39-47. 10.4110/in.2007.7.1.39.
Macrophage Migration Inhibitory Factor (MIF) Induced Stromal Cell-derived Factor 1 (SDF-1) Production Via Nuclear Factor KappaB (NF-kappaB) Signaling in Rheumatoid Arthritis Fibroblast Like Synoviocytes (RA-FLS)
- Affiliations
-
- 1Rheumatism Research Center (RhRC), The Catholic University of Korea, Korea. iammila@catholic.ac.kr
- 2Division of Rheumatology, Department of Medicine, School of Medicine, Konkuk University, Seoul, Korea.
- KMID: 2150626
- DOI: http://doi.org/10.4110/in.2007.7.1.39
Abstract
-
BACKGROUND: Stromal cell-derived factor (SDF)-1 is a potent chemoattractant for activated T cells into the inflamed Rheumatoid arthritis (RA) synovium. To determine the effect of macrophage migration inhibitory factor (MIF) on the production of SDF-1 in the inflamed RA synovium.
METHODS
The expression of SDF-1 and MIF in RA and Osteoarthritis (OA) synovium was examined by immunohistochemical staining. The SDF-1 was quantified by RT-PCR and ELISA after RA fibroblast like synoviocyte (FLS) were treated with MIF in the presence and absence of inhibitors of intracellular signal molecules. The synovial fluid (SF) and serum levels of MIF and SDF-1 in RA, OA and healthy control were measured by ELISA.
RESULTS
Expression of SDF-1 and MIF in synovium was higher in RA patients than in OA patients. The production of SDF-1 was enhanced in RA FLS by MIF stimulation. Such effect of MIF was blocked by the inhibitors of NF-kappaB. Concentrations of SDF-1 in the serum and SF were higher in RA patients than in OA patients and healthy control. SDF-1 and MIF was overexpressed in RA FLS, and MIF could up-regulate the production of SDF-1 in RA FLS via NF-kappaB- mediated pathways.
CONCLUSION
These results suggest that an inhibition of interaction between MIF from T cells and SDF-1 of FLS may provide a new therapeutic approach in the treatment of RA.
Keyword
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- IL-15 Induced an Increased SDF-1 Expression in the Synovial Fibroblasts of Patients with Rheumatoid Arthritis
- Upregulation of Macrophage Migration Inhibitory Factor (MIF) Production by Engagement of Toll-like Receptor 3 (TLR3) on Fibroblast-like Synoviocyte (FLS) from Patients with Rheumatoid Arthritis
- Peroxisome Proliferator-activated Receptor-gamma Agonist Inhibits Pro-inflammatory Gene Expressions and Cellular Proliferation of Fibroblast Like Synoviocytes from Patients with Rheumatoid Arthritis by Down-regulation of NF-kappaB
- Nuclear factor kappaB (NF-kappaB) pathway as a therapeutic target in rheumatoid arthritis
- Rheumatoid Fibroblast-like Synoviocytes Downregulate Foxp3 Expression by Regulatory T Cells Via GITRL/GITR Interaction
