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Dendritic Cell/NK Cell Interaction in RNA Virus Infection

机译:RNA病毒感染中的树突状细胞/ NK细胞相互作用

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Natural killer (NK) cells constitute a major component of the innate immune system and have key roles in early immune responses to pathogens. Although NK cells can be directly activated by pathogens, other sensor cells which recognize pathogen-associated pattern molecules are required for the full activation of NK cells. The NK-activating capacity is observed in myeloid dendritic cells (mDCs), plasmacytoid DCs, macrophages and monocytes. The tropism of the pathogen and the route of invasion influence which sensor cells participate in the NK activation. Influenza virus, measles virus and respiratory syncytial virus can infect human mDCs and induce the ligands of the NK activating receptor NKG2D. Up-regulated NKG2D ligands on mDCs contribute to the mDC-mediated NK activation. By contrast, HCV does not replicate in mDCs and is not an immunostimulatory agent against mDCs. In this case, mDCs are stimulated after detecting dsRNA in the HCV-infected apoptotic hepatocytes via TLR3 and elicit NK activation though a direct cell/cell contact. The TLR3 signal seems to lead the up-regulation of key molecules on the surface membrane of mDCs to enhance NK activity by direct linkage.
机译:天然杀伤(NK)细胞是先天免疫系统的主要组成部分,在对病原体的早期免疫反应中具有关键作用。尽管NK细胞可以被病原体直接激活,但要完全激活NK细胞,就需要其他识别病原体相关模式分子的传感器细胞。在髓样树突细胞(mDC),浆细胞样DC,巨噬细胞和单核细胞中观察到NK激活能力。病原体的嗜性和入侵途径影响哪些传感器细胞参与NK激活。流感病毒,麻疹病毒和呼吸道合胞病毒可以感染人类mDC,并诱导NK激活受体NKG2D的配体。 mDCs上调的NKG2D配体有助于mDC介导的NK激活。相比之下,HCV在mDC中不复制,也不是针对mDC的免疫刺激剂。在这种情况下,通过TLR3在HCV感染的凋亡肝细胞中检测到dsRNA后刺激mDC,并通过直接的细胞/细胞接触引发NK活化。 TLR3信号似乎导致mDCs表面膜上关键分子的上调,从而通过直接键合增强NK活性。

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