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The Korean Association of Immunobiologists (대한면역학회)
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Macrophage Migration Inhibitory Factor (MIF) Induced Stromal Cell-derived Factor 1 (SDF-l) Production Via Nuclear Factor KappaB (NF-${\kappa}B$) Signaling in Rheumatoid Arthritis Fibroblast Like Synoviocytes (RA-FLS)

류마티스관절염 활막세포에서 NF-${\kappa}B$ 신호전달을 통한 MIF의 SDF-1 생성 유도

  • Cho, Mi-La (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Park, Mi-Kyung (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Kim, Kyoung-Woon (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Oh, Hye-Jwa (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Lee, Seon-Yeong (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Park, Jin-Sil (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Heo, Yu-Jung (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Ju, Ji-Hyeon (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Min, Jun-Ki (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Lee, Sang-Heon (Division of Rheumatology, Department of Medicine, School of Medicine, Konkuk University) ;
  • Park, Sung-Hwan (Rheumatism Research Center (RhRC), The Catholic University of Korea) ;
  • Kim, Ho-Youn (Rheumatism Research Center (RhRC), The Catholic University of Korea)
  • 조미라 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 박미경 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 김경운 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 오혜좌 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 이선영 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 박진실 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 허유정 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 주지현 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 민준기 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 이상헌 (건국대학교 의과대학 내과학교실) ;
  • 박성환 (가톨릭대학교 의과대학 류마티스연구센터) ;
  • 김호연 (가톨릭대학교 의과대학 류마티스연구센터)
  • Published : 2007.03.30
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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-${\kappa}B$. 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-${\kappa}B$-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.

Keywords

References

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