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Expression of interleukin-19 in synovial tissue from patients with rheumatoid arthritis

Expression of interleukin-19 in synovial tissue from patients with rheumatoid arthritis
类风湿性关节炎患者滑膜组织中白细胞介素19的表达
批准号:
06670485
负责人:
YAMAMURA Masahiro
金额:
$1.54万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1994
资助国家:
日本
项目状态:
已结题
起止时间:
1994 至 1995

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中文摘要
翻译
探讨白细胞介素-10在类风湿关节炎(RA)中的表达及其致病作用。与骨关节炎患者相比,RA患者血清和滑液中IL-10的浓度更高。RA滑膜组织IL-10 mRNA的表达强于OA,并自发产生更高水平的IL-10。通过免疫组化染色和分离的RA滑膜巨噬细胞、成纤维细胞和T细胞IL-10的检测,内层和亚内层的巨噬细胞都是这种细胞因子的主要来源。IL-10明显抑制RA滑膜产生炎性因子IL-1和TNF-α,但这两种细胞因子是IL-10的强诱导剂。另一方面,T细胞衍生的抗炎细胞因子IL-4和Il-13在抑制滑膜炎症细胞因子方面效率较低,但能够抑制RA滑膜成纤维细胞的增殖。然而,它们在RA关节中的表达非常有限,IL-10的表达与RA中igg -类风湿因子的水平相关。这些结果表明,IL-10可能主要负责RA中慢性炎症和类风湿因子产生的下调,尽管其滑膜表达不足以控制疾病活动。在IL-6型细胞因子中,大量的IL-6、IL-11和LIF主要由IL-1或tnf活化的成纤维细胞产生,而肿瘤抑制素M仅由RA关节的巨噬细胞产生。然而,只有IL-6的循环水平与血清CRP水平升高相关,表明其参与全身炎症反应,如肝脏产生急性pahse反应物。
英文摘要
The expression of interleukin-10 and its pathogenic role in rheumatoid arthritis (RA) was investigated. Concentrations of IL-10 in both serum and synovial fluid from RA patients were greater compared to those of osteoarthritis patients. Synovial tissues in RA more strongly expressed IL-10 mRNA than in OA, and spontaneously produced higher levels of IL-10. By Immunohistochemical staining and detection of IL-10 in isolated macrophages, fibroblasts, and T cells from RA synovium, macrophages in both the lining and sublining layer are major sources of this cytokine. IL-10 markedly inhibited the production of inflammatory cytokines such as IL-1 and TNF-α by RA synovium, but both cytokines were potent inducer of IL-10. On the other hand, T cell-derived anti-inflammatory cytokines, IL-4 and Il-13, are less efficient in inhibiting synovial inflammatory cytokines, 7but are able to inhibit proliferation of RA synovial fibroblasts. However, their expression in RA joint is extremely limited IL-10 expression was associated with levels of IgG-rheumatoid factor in RA. These results indicate that IL-10 may be mostly responsible for downregulation of chronic inflammation and rheumatoid factor production in RA, although its synoival expression if not sufficient to control the disease activity.Of IL-6-type cytokines, large amounts of IL-6, IL-11, and LIF were produced mainly by IL-1 or TNF-activated fibroblasts, whereas oncostatin M was exclusively by macrophages in RA joints. However, only IL-6 was circulating at significant levels in association with raised levels of serum CRP levels, indicating its contribution to systemic inflammatory reactions such as acute-pahse reactant production by liver.
期刊论文(70)
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会议论文
Masahiro Yamamura, Hirofumi Makino: "Cytokine expression of rheumatoid arthritis"Igakuno-ayumi. 182(9). 573-578 (1997)
Masahiro Yamamura、Hirofumi Makino:“类风湿性关节炎的细胞因子表达”Igakuno-ayumi。
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通讯作者:
Yoshitaka Morita, Masahiro Yamamura, Tetsushi Aita, Masanori Kawashima, Seishi Harada, Hideyuki Okamoto, Hajime Inoue, Hirofumi Makino: "Differential Effects of IL-4, IL-10 and IL-13 on Proinflammatory Cytokine Production and Fibroblast Proliferation in V
Yoshitaka Morita、Masahiro Yamamura、Tetsushi Aita、Masanori Kawashima、Seishi Harada、Hideyuki Okamoto、Hajime Inoue、Hirofumi Makino:“IL-4、IL-10 和 IL-13 对 V 中促炎细胞因子产生和成纤维细胞增殖的不同影响
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H,Okamoto.M,Yamamura.Y,Ohmoto.et al.: "Increased production of interleukin-6,leukemia inhibitory factor,and oncostatin M by synovial tissue of rheumatoid arthritis"Arthritis Rheum. 37(9). S382-382 (1994)
H,Okamoto.M,Yamamura.Y,Ohmoto.et al.:“类风湿性关节炎滑膜组织增加白细胞介素 6、白血病抑制因子和制瘤素 M 的产生”关节炎大黄。
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通讯作者:
Kazuhiko Ezawa, Masahiro Yamamura, Hideyuki Okamoto, Zensuke Ota, Hirofumi Makino: "Comparative analysis of CD45RA-and CD45ro-positive CD4ィイD1+ィエD1T cells in peripheral blood, synovial fluid, and synovial tissue in patients with rheumatoid arthritis and a
Kazuhiko Ezawa、Masahiro Yamamura、Hideyuki Okamoto、Zensuke Ota、Hirofumi Makino:“类风湿性关节炎和关节炎患者外周血、滑液和滑液组织中 CD45RA 和 CD45ro 阳性 CD4D1+D1T 细胞的比较分析
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共 45 条
    A study on the molecular mechanism ofcytokine-mediated inhibition of osteoblast differentiation in rheumatoid arthritis
    • 批准号:
      20591178
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.58万
    • 财政年份:
      2008
    • 负责人:
      YAMAMURA Masahiro
    • 依托单位:
    The mechanisms of S100A8/A9-mediated macrophage activation in rheumatoid arthritis
    • 批准号:
      18591111
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.32万
    • 财政年份:
      2006
    • 负责人:
      YAMAMURA Masahiro
    • 依托单位:
    Study on the mechanism for the production of CXCR3-agonisitic chemokines by synovial fibroblasts from patients with rheumatoid arthritis
    • 批准号:
      14570413
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.24万
    • 财政年份:
      2002
    • 负责人:
      YAMAMURA Masahiro
    • 依托单位:
    Study on the mechanism for establishment of the Thl-type immune response in rheumatoid arthritis
    • 批准号:
      12670426
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.05万
    • 财政年份:
      2000
    • 负责人:
      YAMAMURA Masahiro
    • 依托单位:
    海外基金