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本文引用的文献

1
For Whom the Bell Tolls (and Nods): Spit-acular Saliva.《丧钟为谁而鸣》(以及点头):神奇的唾液
Curr Trop Med Rep. 2016 Jun;3(2):40-50. doi: 10.1007/s40475-016-0072-4. Epub 2016 Apr 5.
2
The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation.前列腺素E2-EP3受体轴调节嗜吞噬细胞无形体介导的NLRC4炎性小体激活。
PLoS Pathog. 2016 Aug 2;12(8):e1005803. doi: 10.1371/journal.ppat.1005803. eCollection 2016 Aug.
3
Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores.炎性小体激活的gasdermin D通过形成膜孔导致细胞焦亡。
Nature. 2016 Jul 7;535(7610):153-8. doi: 10.1038/nature18629.
4
Rickettsia australis Activates Inflammasome in Human and Murine Macrophages.澳大利亚立克次氏体激活人和小鼠巨噬细胞中的炎性小体。
PLoS One. 2016 Jun 30;11(6):e0157231. doi: 10.1371/journal.pone.0157231. eCollection 2016.
5
The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation.炎性小体的细胞生物学:炎性小体激活与调控机制
J Cell Biol. 2016 Jun 20;213(6):617-29. doi: 10.1083/jcb.201602089.
6
Pore-forming activity and structural autoinhibition of the gasdermin family.气 分 子 家 族 的 孔 形 成 活 性 和 结 构 自 抑 制 。
Nature. 2016 Jul 7;535(7610):111-6. doi: 10.1038/nature18590. Epub 2016 Jun 8.
7
Inflammasome Complexes: Emerging Mechanisms and Effector Functions.炎性小体复合物:新出现的机制与效应功能
Cell. 2016 May 5;165(4):792-800. doi: 10.1016/j.cell.2016.03.046.
8
NLRP3 recruitment by NLRC4 during Salmonella infection.沙门氏菌感染期间NLRC4对NLRP3的招募
J Exp Med. 2016 May 30;213(6):877-85. doi: 10.1084/jem.20132234. Epub 2016 May 2.
9
The Tick Protein Sialostatin L2 Binds to Annexin A2 and Inhibits NLRC4-Mediated Inflammasome Activation.蜱蛋白唾液酸抑制素L2与膜联蛋白A2结合并抑制NLRC4介导的炎性小体激活。
Infect Immun. 2016 May 24;84(6):1796-1805. doi: 10.1128/IAI.01526-15. Print 2016 Jun.
10
Innate Immunity Holding the Flanks until Reinforced by Adaptive Immunity against Mycobacterium tuberculosis Infection.固有免疫在抗结核分枝杆菌感染的适应性免疫增强之前坚守侧翼防线。
Front Microbiol. 2016 Mar 14;7:328. doi: 10.3389/fmicb.2016.00328. eCollection 2016.

异常行为:蜱传病原体与炎性小体信号传导

Deviant Behavior: Tick-Borne Pathogens and Inflammasome Signaling.

作者信息

Shaw Dana K, McClure Erin E, Wang Xiaowei, Pedra Joao H F

机构信息

Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

出版信息

Vet Sci. 2016 Sep 28;3(4):27. doi: 10.3390/vetsci3040027.

DOI:10.3390/vetsci3040027
PMID:29056735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5606592/
Abstract

In the face of an assault, host cells mount an immediate response orchestrated by innate immunity. Two of the best described innate immune signaling networks are the Toll- and the Nod-like receptor pathways. Extensive work has been done characterizing both signaling cascades with several recent advances on the forefront of inflammasome biology. In this review, we will discuss how more commonly-studied pathogens differ from tick-transmitted microbes in the context of Nod-like receptor signaling and inflammasome formation. Because pathogens transmitted by ticks have unique characteristics, we offer the opinion that these microbes can be used to uncover novel principles of Nod-like receptor biology.

摘要

面对攻击时,宿主细胞会启动由先天免疫精心编排的即时反应。两个描述得最为详尽的先天免疫信号网络是Toll样受体途径和Nod样受体途径。在炎症小体生物学前沿领域有多项最新进展,针对这两种信号级联反应已经开展了大量研究。在本综述中,我们将讨论在Nod样受体信号传导和炎症小体形成的背景下,研究更为普遍的病原体与蜱传微生物有何不同。由于蜱传播的病原体具有独特特征,我们认为这些微生物可用于揭示Nod样受体生物学的新原理。