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人白介素1β轉(zhuǎn)換酶（ICE）elisa試劑盒

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Background Patients with rheumatoid arthritis （RA） have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 （IL-17） contributes to this defect.

人白介素1β轉(zhuǎn)換酶（ICE）elisa試劑盒產(chǎn)品信息

Background Patients with rheumatoid arthritis (RA) have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 (IL-17) contributes to this defect. Methods IL-17 effects on Th1 markers were examined on T-bet and interferon γ (IFNγ) expression in peripheral blood mononuclear cells (PBMCs) from patients with RA or healthy controls (HC). Receptor specificities were determined by analysis of the Th1-specific IL-12 receptor β2 (IL-12Rβ2), Th17-specific IL-23R and the common IL-12Rβ1 chain expression. Effects of IL-17 or IFNγ on IL-6, IL-1, IL-8, matrix metalloproteinase-8 (MMP-8) were measured by real-time RT-PCR in RA synovial cells. Results RA PBMCs were less responsive to IL-12-induced IFNγ than HC PBMCs. IL-12 hyporesponsiveness was increased by IL-17 treatment associated with a selective reduction in IL-12Rβ2, but not IL-23R, IL-12Rβ1 or T-bet, which was reversed with IL-17R inhibition. IL-17 inhibited IL-12Rβ2 expression in developing Th1 cells. In RA synovial cells, IL-17 induced IL-6, IL-1, IL-8 and MMP-8, whereas IFNγ haBackground Patients with rheumatoid arthritis (RA) have a systemic Th1 defect associated with inflammation. Objective To examine the hypothesis that interleukin 17 (IL-17) contributes to this defect. Methods IL-17 effects on Th1 markers were examined on T-bet and interferon γ (IFNγ) expression in peripheral blood mononuclear cells (PBMCs) from patients with RA or healthy controls (HC). Receptor specificities were determined by analysis of the Th1-specific IL-12 receptor β2 (IL-12Rβ2), Th17-specific IL-23R and the common IL-12Rβ1 chain expression. Effects of IL-17 or IFNγ on IL-6, IL-1, IL-8, matrix metalloproteinase-8 (MMP-8) were measured by real-time RT-PCR in RA synovial cells. Results RA PBMCs were less responsive to IL-12-induced IFNγ than HC PBMCs. IL-12 hyporesponsiveness was increased by IL-17 treatment associated with a selective reduction in IL-12Rβ2, but not IL-23R, IL-12Rβ1 or T-bet, which was reversed with IL-17R inhibition. IL-17 inhibited IL-12Rβ2 expression in developing Th1 cells. In RA synovial cells, IL-17 induced IL-6, IL-1, IL-8 and MMP-8, whereas IFNγ ha