IMMUNE NETWORK
- 제3권4호
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- Pages.310-319
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- 2003
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- 1598-2629(pISSN)
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- 2092-6685(eISSN)
류마티스 관절염 환자의 말초혈액 단핵세포에서 Phosphoinositide 3-Kinase (PI3K)/Akt와 Nuclear Factor KappaB (NF-κB) 신호전달을 통한 IL-17 생성조절
Regulation of Interleukin-17 Production in Patients with Rheumatoid Arthritis by Phosphoinositide 3-kinase (PI3K)/Akt and Nuclear Factor KappaB (NF-κB) Dependent Signal Transduction Pathway
- 김경운 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 조미라 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 이상헌 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 민소연 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 박미경 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 박성환 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 주대명 (가톨릭대학교 의과학연구원 류마티스연구센터) ;
- 김호연 (가톨릭대학교 의과학연구원 류마티스연구센터)
- Kim, Kyoung-Woon (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Cho, Mi-La (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Lee, Sang-Heon (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Min, So-Youn (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Park, Mi Kyung (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Park, Sung-Hwan (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Jue, Dae-Myung (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea) ;
- Kim, Ho-Youn (Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea)
- 발행 : 2003.12.30
초록
Inflammatory mediators has been recognized as an important role in the pathogenesis of rheumatoid arthritis (RA). IL-17 is increasingly recognized as an important regulator of immune and inflammatory responses, including induction of proinflammatory cytokines and osteoclastic bone resorption. Evidence of the expression and proinflammatory activity of IL-17 has been demonstrated in RA synovium and in animal models of RA. However, the signaling pathways that regulate IL-17 production remain unknown. In the present study, we investigated the role of the phosphatidylinositol 3 kinase (PI3K)-Akt pathway in the regulation of IL-17 production in RA. PBMC were separated from RA (n=24) patients, and stimulated with various agents (anti CD3, anti CD28, PHA, ConA, IL-15). IL-17 levels were determined by sandwich ELISA and RT-PCR. The production of IL-17 was significantly increased in cells treated with anti-CD3 antibody, PHA, IL-15 or MCP-1 (P<0.05). ConA also strongly induced IL-17 production (P<0.001), whereas TNF-alpha, IL-1beta, IL-18 or TGF-beta did not. IL-17 was detected in the PBMC of patients with osteoarthritis (OA) but their expression levels were much lower than those of RA PBMC. Anti-CD3 antibody activated the PI3K-Akt pathway and activation of the PI3K-Akt pathway resulted in a pronounced augmentation of nuclear factor kappaB (