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Direct effects of activin A on the activation of mouse macrophage RAW264.7 cells
  • ISSN号:1672-7681 (Print)
  • 期刊名称:Cell Mol Immunol
  • 时间:0
  • 页码:129-133
  • 语言:中文
  • 分类:R285.1[医药卫生—中药学;医药卫生—中医学] R282.71[医药卫生—中药学;医药卫生—中医学]
  • 作者机构:[1]Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, China, [2]Department of Surgery, China-Japan Union Hospital, Jilin University Changchun 130031, China
  • 相关基金:This work was supported by grants from the Natural Science Foundation of China (30671953 and 30801005) and Ministry of Education of China (No. 20070183013).
  • 相关项目:LFA-1(CD11a)在类风湿性关节炎发生、发展中的作用机制研究
中文摘要:

巨噬细胞经由 secreting 支持 inflammatory 调停人, phagocytosing 微生物和介绍抗原在天生的有免疫力、获得的免疫者起关键作用。Activin A,转变生长因素(TGF-) 总科的一个成员,被巨噬细胞和 microglia 细胞生产。在这研究,我们在老鼠巨噬细胞房间线 RAW264.7 房间上作为一个支持 inflammatory 因素报导了 activin A 的直接效果。我们的数据表明 activin A 不能仅仅从 RAW264.7 房间增加 IL-1 和 IL-6 生产,而且支持 pinocytic 和 RAW264.7 房间的吞噬细胞的活动。另外, activin A RAW264.7 房间的表面上的显然起来调整的 MHC II 表示,而没影响 MHC 我表示。Activin A 也提高了 CD80 表示,它是激活的巨噬细胞的一个标记,但是没影响 RAW264.7 房间增长。这些数据建议 activin A 可以经由支持休息巨噬细胞的激活调整主要调停巨噬细胞的天生、获得的有免疫力的反应。

英文摘要:

Macrophages play critical roles in innate immune and acquired immune v/a secreting pro-inflammatory mediators, phagocytosing microorganisms and presenting antigens. Activin A, a member of transforming growth factor (TGF-β) superfamily, is produced by macrophages and microglia cells. In this study, we reported a direct effect of activin A as a pro-inflammatory factor on mouse macrophage cell line RAW264.7 cells. Our data revealed that activin A could not only increase IL-1β and IL-6 production from RAW264.7 cells, but also promote pinocytic and phagocytic activities of RAW264.7 cells. In addition, activin A obviously up-regulated MHC Ⅱ expression on the surface of RAW264.7 cells, whereas did not influence MHC I expression. Activin A also enhanced CD80 expression, which is a marker of activated macrophages, but did not influence RAW264.7 cell proliferation. These data suggest that activin A may regulate primary macrophage-mediated innate and acquired immune response via promoting the activation of rest macrophages.

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