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本文引用的文献

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Type I IFN triggers RIG-I/TLR3/NLRP3-dependent inflammasome activation in influenza A virus infected cells.Ⅰ型干扰素在甲型流感病毒感染细胞中触发 RIG-I/TLR3/NLRP3 依赖性炎性小体激活。
PLoS Pathog. 2013;9(4):e1003256. doi: 10.1371/journal.ppat.1003256. Epub 2013 Apr 11.
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Receptor interacting protein kinase 2-mediated mitophagy regulates inflammasome activation during virus infection.受体相互作用蛋白激酶 2 介导线粒体自噬调节病毒感染期间的炎症小体激活。
Nat Immunol. 2013 May;14(5):480-8. doi: 10.1038/ni.2563. Epub 2013 Mar 24.
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Rabies virus is recognized by the NLRP3 inflammasome and activates interleukin-1β release in murine dendritic cells.狂犬病病毒被 NLRP3 炎性小体识别,并在小鼠树突状细胞中激活白细胞介素-1β释放。
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Herpes simplex virus 1 infection induces activation and subsequent inhibition of the IFI16 and NLRP3 inflammasomes.单纯疱疹病毒 1 感染诱导 IFI16 和 NLRP3 炎性小体的激活和随后的抑制。
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The protein kinase PKR is critical for LPS-induced iNOS production but dispensable for inflammasome activation in macrophages.蛋白激酶 PKR 对于 LPS 诱导的 iNOS 产生至关重要,但对于巨噬细胞中的炎性体激活是可有可无的。
Eur J Immunol. 2013 May;43(5):1147-52. doi: 10.1002/eji.201243187. Epub 2013 Mar 15.
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ATP release and purinergic signaling in NLRP3 inflammasome activation.三磷酸腺苷释放和嘌呤能信号在 NLRP3 炎性小体激活中的作用。
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NLRs 在抗病毒免疫中的作用不断扩大。

The expanding role of NLRs in antiviral immunity.

机构信息

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105-3678, USA.

出版信息

Immunol Rev. 2013 Sep;255(1):13-24. doi: 10.1111/imr.12089.

DOI:10.1111/imr.12089
PMID:23947344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3759815/
Abstract

Nucleotide oligomerization and binding domain (NOD)-like receptors (NLRs) are a major constituent of the cytosolic innate immune-sensing machinery and participate in a wide array of pathways including nuclear factor κB (NF-κB), mitogen-activated protein kinase (MAPK), inflammasome, and type I interferon (IFN) signaling. NLRs have known roles in autoimmune, autoinflammatory, and infectious diseases. With respect to virus infection, NLRP3 is the most extensively studied NLR, including mechanisms of activation and inhibition. Furthermore, the importance of NLRP3 in both innate and adaptive immunity has been demonstrated. In comparison to NLRP3, the roles of other NLRs during virus infection are only just emerging. NLRC2 is an important activator of innate antiviral signaling and was recently found to mitigate inflammation during virus infection through autophagy. Finally, functions for NLRX1 in immune modulation and reactive oxygen species production require further examination and the importance of NLRC5 as a transactivator of major histocompatibility complex (MHC) class I and antigen presentation is currently developing. In this review, we discuss current knowledge pertaining to viruses and NLRs as well as areas of potential research, which will help advance the study of NLR biology during virus infection.

摘要

核苷酸寡聚化和结合域 (NOD)-样受体 (NLRs) 是细胞溶质先天免疫感应机制的主要组成部分,参与包括核因子 κB (NF-κB)、丝裂原激活蛋白激酶 (MAPK)、炎性体和 I 型干扰素 (IFN) 信号在内的广泛途径。NLRs 在自身免疫、自身炎症和感染性疾病中具有已知作用。就病毒感染而言,NLRP3 是研究最广泛的 NLR,包括激活和抑制机制。此外,NLRP3 在先天和适应性免疫中的重要性已得到证实。与 NLRP3 相比,其他 NLR 在病毒感染期间的作用才刚刚出现。NLRC2 是先天抗病毒信号的重要激活剂,最近发现它通过自噬减轻病毒感染期间的炎症。最后,NLRX1 在免疫调节和活性氧产生中的功能需要进一步检查,NLRC5 作为主要组织相容性复合体 (MHC) 类 I 和抗原呈递的转激活因子的重要性目前正在发展。在这篇综述中,我们讨论了与病毒和 NLR 相关的现有知识以及潜在的研究领域,这将有助于推进病毒感染期间 NLR 生物学的研究。