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김경운,조미라,이상헌,민소연,박미경,박성환,주대명,김호연,Kim, Kyoung-Woon,Cho, Mi-La,Lee, Sang-Heon,Min, So-Youn,Park, Mi Kyung,Park, Sung-Hwan,Jue, Dae-Myung,Kim, Ho-Youn 대한면역학회 2003 Immune Network Vol.3 No.4
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 ($NF-{\kappa}B$). IL-17 production by activated PBMC in RA is completely or partially blocked in the presence of $NF-{\kappa}B$ inhibitor PDTC and PI3K-Akt inhibitor, wortmannin and LY294002, respectively. Whereas the inhibition of AP-1 and extracellular signal-regulated kinase (ERK)1/2 did not affect IL-17 production. These results provide new insight into that PI3K/Akt and $NF-{\kappa}B$ dependent signal transduction pathway could be involved in the overproduction of key inflammatory cytokine, IL-17 in rheumatoid arthritis.
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류마티스 질환에서 혈청 Soluble Fas Ligand (sFasL), FasL-Fas 복합체, FasL-IgG 복합체 측정
민준기 ( Jun Ki Min ),민소연 ( So Youn Min ),조미라 ( Mi Ra Cho ),정재연 ( Jae Yeon Jeong ),주대명 ( Dae Myung Jue ),민도준 ( Do June Min ),조철수 ( Chul Soo Cho ),김호연 ( Ho Youn Kim ) 대한류마티스학회 2000 대한류마티스학회지 Vol.7 No.4
Objective: To quantify the soluble Fas ligand (sFasL) and to measure FasL-Fas complex and FasL-IgG complex in the sera of patients with various rheumatic diseases: systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), and adult onset Still`s disease (AOSD). Methods: Serum samples were obtained from 37 patients with SLE, 40 with RA, 30 with SSc, 20 with AOSD, and 40 healthy controls. The serum sFasL, FasL-Fas complex, and FasL-IgG complex were measured using a sandwich enzyme-linked immunoabsorbent assay. Hospital medical records were retrospectively reviewed for clinical and laboratory characteristics in patients with SLE. Disease activity in SLE patients was assessed by the SLE Disease Activity Index (SLEDAI) score. Results: In patients with SLE, serum sFasL levels (383.1±208.9pg/ml) were significantly higher (p<0.001) than those of healthy controls (192.0±84.7pg/ml). sFasL levels in patients with RA (150.8±30.7pg/ml, p=0.014), SSc (115.4±13.5pg/ml, p<0.001), and AOSD (137.5±12.9pg/ml, p=0.001) were significantly lower compared with healthy controls. The frequencies of positive FasL-Fas complex and FasL-IgG complex were higher in patients with SLE (56.8%, 56.8% respectively) than in healthy controls (2.5%, 0% respectively) (p<0.001). All patients with RA or AOSD were negative for FasL-Fas complex and FasL-IgG complex. No patients with SSc were positive for FasL-Fas complex. On the other hand, the positive frequency of FasL-IgG complex was greater in patients with SSc (16.7%) than in healthy controls (0%) (p=0.012). Serum levels of FasL-IgG complexes in active SLE patients (OD 0.467±0.050) were tended to be lower than those in inactive SLE patients (OD 0.509±0.055) (p=0.060). SLEDAI score was tended to be negatively correlated with the serum levels of FasL-IgG complex in patients with SLE (r=-0.308, p=0.068). Conclusion: These results suggest that FasL may possibly play a role in the pathogenesis of SLE.
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