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C型凝集素DC-SIGN介导的碳水化合物信号传导影响核因子κB活性。

Carbohydrate signaling by C-type lectin DC-SIGN affects NF-kappaB activity.

作者信息

Gringhuis Sonja I, Geijtenbeek Teunis B H

机构信息

Center of Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

出版信息

Methods Enzymol. 2010;480:151-64. doi: 10.1016/S0076-6879(10)80008-4.

Abstract

Pathogen recognition is central to the induction of adaptive immunity. Dendritic cells (DCs) express different pattern recognition receptors (PRRs), such as Toll-like receptors and C-type lectins, that sense invading pathogens. Pathogens trigger a specific set of PRRs, leading to activation of intracellular signaling processes that shapes the adaptive immunity. It is becoming clear that cross talk between these signaling routes is crucial for pathogen-tailored immune responses. The C-type lectin DC-SIGN interacts with different mannose-expressing pathogens such as Mycobacterium tuberculosis and HIV-1. Notably, DC-SIGN triggering by these pathogens results in a specific Raf-1-dependent signaling pathway that modulates TLR-induced NF-kappaB activation. Here, we will discuss the various methods that we have used to identify the innate signaling by the C-type lectin DC-SIGN, and how to analyze the consequences on NF-kappaB activation.

摘要

病原体识别是诱导适应性免疫的核心。树突状细胞(DC)表达不同的模式识别受体(PRR),如Toll样受体和C型凝集素,可感知入侵的病原体。病原体触发特定的一组PRR,导致细胞内信号传导过程的激活,从而塑造适应性免疫。越来越清楚的是,这些信号通路之间的相互作用对于针对病原体的免疫反应至关重要。C型凝集素DC-SIGN与不同的表达甘露糖的病原体相互作用,如结核分枝杆菌和HIV-1。值得注意的是,这些病原体触发DC-SIGN会导致特定的依赖Raf-1的信号通路,该通路调节TLR诱导的NF-κB激活。在这里,我们将讨论我们用于识别C型凝集素DC-SIGN的固有信号传导的各种方法,以及如何分析对NF-κB激活的影响。

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