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首页> 外文期刊>Nature immunology >Inflammatory mediators are insufficient for full dendritic cell activation and promote expansion of CD4(+) T cell populations lacking helper function
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Inflammatory mediators are insufficient for full dendritic cell activation and promote expansion of CD4(+) T cell populations lacking helper function

机译:炎性介质不足以完全激活树突状细胞并促进缺乏辅助功能的CD4(+)T细胞群体的扩张

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摘要

Dendritic cells (DCs) can be activated directly by triggering of receptors for pathogens or, indirectly, by exposure to inflammatory signals. It remains unclear, however, whether the two pathways result in qualitatively similar DCs or lead to equivalent adaptive immune responses. Here we report that indirect activation by inflammatory mediators generated DCs that supported CD4(+) T cell clonal expansion but failed to direct T helper cell differentiation. In contrast, exposure to pathogen components resulted in fully activated DCs that promoted T helper responses. These results indicate that inflammation cannot substitute for contact with pathogen components in DC activation and suggest that the function of pattern recognition by DCs is to couple the quality of the adaptive immune response to the nature of the pathogen.
机译:树突状细胞(DC)可以通过触发病原体的受体直接激活,或通过暴露于炎症信号而间接激活。然而,尚不清楚这两种途径是否导致定性相似的DC或导致等效的适应性免疫应答。在这里我们报告说,炎症介质的间接激活产生了支持CD4(+)T细胞克隆扩增但未能指导T辅助细胞分化的DC。相反,暴露于病原体成分​​会导致DC完全活化,从而促进T辅助反应。这些结果表明炎症不能替代与DC激活中的病原体成分​​接触,并表明DC识别模式的功能是将适应性免疫反应的质量与病原体的性质相结合。

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