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本文引用的文献

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Molecular mechanism of NLRP3 inflammasome activation.NLRP3 炎性体激活的分子机制。
J Clin Immunol. 2010 Sep;30(5):628-31. doi: 10.1007/s10875-010-9440-3. Epub 2010 Jun 30.
2
Influenza virus activates inflammasomes via its intracellular M2 ion channel.流感病毒通过其细胞内的 M2 离子通道激活炎症小体。
Nat Immunol. 2010 May;11(5):404-10. doi: 10.1038/ni.1861. Epub 2010 Apr 11.
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The inflammasomes.炎症小体。
Cell. 2010 Mar 19;140(6):821-32. doi: 10.1016/j.cell.2010.01.040.
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The NLRP3 inflammasome, a target for therapy in diverse disease states.NLRP3 炎性小体，一种针对多种疾病状态的治疗靶点。
Eur J Immunol. 2010 Mar;40(3):631-4. doi: 10.1002/eji.200940162.
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Critical functions of priming and lysosomal damage for NLRP3 activation.引发和溶酶体损伤对 NLRP3 激活的关键作用。
Eur J Immunol. 2010 Mar;40(3):620-3. doi: 10.1002/eji.200940185.
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NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production?NLRP3 炎性小体激活：ROS 产生的多种信号通路汇聚？
Nat Rev Immunol. 2010 Mar;10(3):210-5. doi: 10.1038/nri2725. Epub 2010 Feb 19.
7
Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production.RIG-I 通过识别 RNA 病毒激活 CARD9 和炎症小体信号通路，从而产生白细胞介素 1β。
Nat Immunol. 2010 Jan;11(1):63-9. doi: 10.1038/ni.1824. Epub 2009 Nov 15.
8
The intracellular sensor NLRP3 mediates key innate and healing responses to influenza A virus via the regulation of caspase-1.细胞内传感器NLRP3通过调节半胱天冬酶-1介导对甲型流感病毒的关键先天性和愈合反应。
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9
The NLRP3 inflammasome mediates in vivo innate immunity to influenza A virus through recognition of viral RNA.NLRP3炎性小体通过识别病毒RNA介导机体对甲型流感病毒的天然免疫。
Immunity. 2009 Apr 17;30(4):556-65. doi: 10.1016/j.immuni.2009.02.005. Epub 2009 Apr 9.
10
The inflammasomes: guardians of the body.炎性小体：身体的守护者。
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细胞内 poly I:C 激活 NLRP3 炎性小体。

Activation of the NLRP3 inflammasome by intracellular poly I:C.

机构信息

Institute for Systems Biology, Seattle, WA 98103, USA.

出版信息

FEBS Lett. 2010 Nov 19;584(22):4627-32. doi: 10.1016/j.febslet.2010.10.036. Epub 2010 Oct 23.

DOI:10.1016/j.febslet.2010.10.036
PMID:20971108
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3005299/
Abstract

Several RNA viruses can be detected by the inflammasome, which promotes IL-1β and IL-18 secretion, but the underlying mechanisms of detection remain unclear. Cytosolic dsRNA is a replication intermediate of many RNA viruses. We show here that transfection of the dsRNA analogue poly I:C activates the NLRP3 inflammasome via a pathway requiring endosomal acidification. This detection is independent of the other poly I:C sensors: TLR3 and MDA5. These results suggest a mechanism by which cytosolic dsRNA produced during viral infection could activate the NLRP3 inflammasome.

摘要

几种 RNA 病毒可以被炎症小体检测到，炎症小体促进白细胞介素 1β 和白细胞介素 18 的分泌，但检测的潜在机制尚不清楚。细胞质双链 RNA 是许多 RNA 病毒的复制中间体。我们在这里表明，双链 RNA 类似物聚肌胞的转染通过需要内体酸化的途径激活 NLRP3 炎症小体。这种检测不依赖于其他聚肌胞传感器：TLR3 和 MDA5。这些结果表明，在病毒感染过程中产生的细胞质双链 RNA 可以激活 NLRP3 炎症小体的一种机制。