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CCL20 在感染结核分枝杆菌的单核细胞中过表达,并抑制活性氧(ROS)的产生。

CCL20 is overexpressed in Mycobacterium tuberculosis-infected monocytes and inhibits the production of reactive oxygen species (ROS).

机构信息

Fundación Instituto de Estudios de Ciencias de la Salud de Castilla y León, Hospital de León, Spain.

出版信息

Clin Exp Immunol. 2010 Nov;162(2):289-97. doi: 10.1111/j.1365-2249.2010.04168.x. Epub 2010 Sep 1.

Abstract

CCL20 is a chemokine that attracts immature dendritic cells. We show that monocytes, cells characteristic of the innate immune response, infected with Mycobacterium tuberculosis express the CCL20 gene at a much higher level than the same cells infected with non-tuberculous mycobacteria. Interferon (IFN)-γ, a fundamental cytokine in the immune response to tuberculosis, strongly inhibits both the transcription and the translation of CCL20. We have also confirmed that dendritic cells are a suitable host for mycobacteria proliferation, although CCL20 does not seem to influence their intracellular multiplication rate. The chemokine, however, down-regulates the characteristic production of reactive oxygen species (ROS) induced by M. tuberculosis in monocytes, which may affect the activity of the cells. Apoptosis mediated by the mycobacteria, possibly ROS-dependent, was also inhibited by CCL20.

摘要

CCL20 是一种趋化因子,可吸引未成熟的树突状细胞。我们发现,与感染非结核分枝杆菌的细胞相比,感染结核分枝杆菌的单核细胞(固有免疫反应的特征细胞)表达 CCL20 基因的水平要高得多。IFN-γ 是针对结核病的免疫反应中的一种基本细胞因子,它强烈抑制 CCL20 的转录和翻译。我们还证实,树突状细胞是分枝杆菌增殖的合适宿主,尽管 CCL20 似乎不会影响其细胞内倍增率。然而,趋化因子下调了单核细胞中由结核分枝杆菌诱导的活性氧物质(ROS)的特征产生,这可能会影响细胞的活性。分枝杆菌介导的细胞凋亡(可能依赖于 ROS)也被 CCL20 抑制。

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