单核细胞化学引诱物蛋白1释放葡糖氨基葡聚糖调节其profibrotic影响系统性硬化症通过释放interleukin-4从T细胞。
文章的细节
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引用
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Distler JH, Jungel Caretto D, Schulze-Horsel U, Kowal-Bielecka啊,同性恋再保险,米歇尔•巴Muller-Ladner U, Kalden JR,同性恋,Distler O
单核细胞化学引诱物蛋白1释放葡糖氨基葡聚糖调节其profibrotic影响系统性硬化症通过释放interleukin-4从T细胞。
关节炎感冒。2006年1月,54 (1):214 - 25。
- PubMed ID
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16385517 (在PubMed]
- 文摘
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摘要目的:单核细胞化学引诱物蛋白1 (MCP-1;CCL2)与纤维化疾病的发病机理和上调患者系统性硬化症(SSc)。本研究的目的是检查机制MCP-1介导其profibrotic SSc设置的影响。方法:MCP-1真皮成纤维细胞上的受体的表达进行了分析通过实时聚合酶链反应和fluorescence-activated细胞排序。细胞外基质蛋白的结合和释放MCP-1量化了酶联免疫吸附试验。使用magnetic-activated Th0细胞被孤立的细胞分类系统和刺激两次MCP-1的存在。胶原蛋白的合成使用Sircol胶原蛋白分析工具测量。结果:粘多糖硫酸软骨素,但不是纤连蛋白或胶原蛋白、绑定和MCP-1发布时间的方式。MCP-1释放从硫酸软骨素的分化诱导interleukin-4生成(il - 4)的T细胞通常可以剂量依赖性的方式。反过来,从患者SSc真皮成纤维细胞表达il - 4受体刺激和il - 4显著增加真皮成纤维细胞胶原蛋白的生产。 In contrast, CCR2a and CCR2b, as well as D6 and US28 (other potential receptors of MCP-1), were not detectable in SSc and normal fibroblasts, and their expression was not induced by platelet-derived growth factor, IL-1beta, or IL-4. In addition, MCP-1 had no direct effects on collagen production by fibroblasts. CONCLUSION: MCP-1 has no direct effects on dermal fibroblasts but contributes to fibrosis in patients with SSc by inducing the differentiation of IL-4-producing T cells. Because MCP-1 has both proinflammatory and profibrotic effects, pharmacologic targeting of MCP-1 could be a promising therapeutic approach in SSc.