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首页> 外文期刊>Medical Microbiology and Immunology >The CFP-10/ESAT-6 complex of Mycobacterium tuberculosis potentiates the activation of murine macrophages involvement of IFN-gamma signaling.
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The CFP-10/ESAT-6 complex of Mycobacterium tuberculosis potentiates the activation of murine macrophages involvement of IFN-gamma signaling.

机译:结核分枝杆菌的CFP-10 / ESAT-6复合物增强了鼠巨噬细胞对IFN-γ信号传导的激活。

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摘要

Secretory antigen of Mycobacterium tuberculosis, culture filtered protein 10(CFP-10) and early secreted antigenic target 6 kDa protein (ESAT-6) are closely correlated with immunogenicity and virulence of Mycobacterium tuberculosis. But the mechanism of its immunogenicity and virulence is still unclear. In this study, we investigated the influence of the CFP-10/ESAT-6 complex on production of IL-12 and nitric oxide (NO) produced by the ANA-1 macrophage cell line. Preincubation with the complex in a time-dependent manner significantly enhanced production of NO and IL-12 released from ANA-1 cells following IFN-gamma stimulation. In addition, the complex up-modulated expression level of IFN-gammaR1 on surface of the macrophages. Furthermore, the effect of the complex on production of IL-12 and NO in ANA-1 cells was suppressed by AG490, a selective inhibitor of JAK/STAT pathway. These data suggest that in the presence of IFN-gamma, CFP-10/ESAT-6 complex represents a new immunogenicity and protective factor that may be, at least partly, due to up modulation of IFN-gammaR1 expression and activation of JAK/STAT pathway.
机译:结核分枝杆菌的分泌抗原,培养物过滤蛋白10(CFP-10)和早期分泌的抗原靶标6 kDa蛋白(ESAT-6)与结核分枝杆菌的免疫原性和毒力密切相关。但是其免疫原性和毒力的机制仍不清楚。在这项研究中,我们调查了CFP-10 / ESAT-6复合物对ANA-1巨噬细胞系产生的IL-12和一氧化氮(NO)的影响。与复合物的预温育以时间依赖性方式显着增强了在IFN-γ刺激后从ANA-1细胞释放的NO和IL-12的产生。另外,巨噬细胞表面上IFN-γR1的表达水平被复杂地上调。此外,该复合物对ANA-1细胞中IL-12和NO产生的影响被AG490(JAK / STAT途径的选择性抑制剂)抑制。这些数据表明,在存在IFN-γ的情况下,CFP-10 / ESAT-6复合物代表了一种新的免疫原性和保护因子,这可能至少部分是由于IFN-γR1表达的上调和JAK / STAT的激活途径。

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