IL-18 is produced by articular chondrocytes and induces proinflammatory and catabolic responses.

IL-18 is produced by articular chondrocytes and induces proinflammatory and catabolic responses.
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DOI:
10.4049/jimmunol.162.2.1096
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发表时间:
1999-01
影响因子:
4.4
通讯作者:
T. Olee;S. Hashimoto;J. Quach;M. Lotz
T. Olee;S. Hashimoto;J. Quach;M. Lotz
中科院分区:
医学2区
文献类型:
--
作者:
T. Olee;S. Hashimoto;J. Quach;M. Lotz

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IL-18是一种最初被鉴定为IFN-γ诱导因子的细胞因子,是IL-1蛋白家族的成员。由于IL-1 α和IL-1 β是关节炎发病机制中的重要介质,因此本研究探讨了IL-18在关节软骨细胞中的表达及其调节作用。IL-1 β诱导软骨细胞IL-18 mRNA表达。软骨细胞产生IL-18前体,并响应于IL-1刺激分泌成熟形式的IL-18。关于IL-18对软骨细胞作用的研究表明,它抑制TGF-β诱导的增殖并增强一氧化氮的产生。IL-18刺激正常人关节软骨细胞中几种基因的表达,包括诱导型一氧化氮合酶、诱导型环氧合酶、IL-6和基质溶解素。基因表达与相应蛋白质的合成有关。用IL-18处理正常人关节软骨增加了糖胺聚糖的释放。这些发现将IL-18鉴定为调节软骨细胞反应并促进软骨降解的细胞因子。
IL-18, a cytokine originally identified as IFN-gamma-inducing factor, is a member of the IL-1 family of proteins. Because IL-1alpha and IL-1beta are important mediators in the pathogenesis of arthritis, the present study addresses the expression of IL-18 and its role in regulating in articular chondrocytes. IL-18 mRNA was induced by IL-1beta in chondrocytes. Chondrocytes produced the IL-18 precursor and in response to IL-1 stimulation secreted the mature form of IL-18. Studies on IL-18 effects on chondrocytes showed that it inhibits TGF-beta-induced proliferation and enhances nitric oxide production. IL-18 stimulated the expression of several genes in normal human articular chondrocytes including inducible nitric oxide synthase, inducible cyclooxygenase, IL-6, and stromelysin. Gene expression was associated with the synthesis of the corresponding proteins. Treatment of normal human articular cartilage with IL-18 increased the release of glycosaminoglycans. These finding identify IL-18 as a cytokine that regulates chondrocyte responses and contributes to cartilage degradation.