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本文引用的文献

1
The complement system facilitates clearance of Enterococcus faecium during murine peritonitis.补体系统有助于清除腹膜炎期间的粪肠球菌。
J Infect Dis. 2010 Feb 15;201(4):544-52. doi: 10.1086/650341.
2
Theiler's virus infection chronically alters seizure susceptibility.西勒氏病毒感染会慢性改变癫痫易感性。
Epilepsia. 2010 Aug;51(8):1418-28. doi: 10.1111/j.1528-1167.2009.02405.x. Epub 2009 Dec 1.
3
Role of neutrophils, MyD88-mediated neutrophil recruitment, and complement in antibody-mediated defense against Pseudomonas aeruginosa keratitis.中性粒细胞的作用、MyD88 介导的中性粒细胞募集和补体在抗假单胞菌角膜炎中的抗体介导防御作用。
Invest Ophthalmol Vis Sci. 2010 Apr;51(4):2085-93. doi: 10.1167/iovs.09-4139. Epub 2009 Nov 5.
4
Innate but not adaptive immune responses contribute to behavioral seizures following viral infection.先天而非适应性免疫反应有助于病毒感染后的行为性癫痫发作。
Epilepsia. 2010 Mar;51(3):454-64. doi: 10.1111/j.1528-1167.2009.02390.x. Epub 2009 Oct 20.
5
Apoptosis of hippocampal pyramidal neurons is virus independent in a mouse model of acute neurovirulent picornavirus infection.在急性神经毒性微小核糖核酸病毒感染的小鼠模型中,海马锥体神经元的凋亡与病毒无关。
Am J Pathol. 2009 Aug;175(2):668-84. doi: 10.2353/ajpath.2009.081126. Epub 2009 Jul 16.
6
The complement cascade: Yin-Yang in neuroinflammation--neuro-protection and -degeneration.补体级联反应:神经炎症中的阴阳——神经保护与神经退变
J Neurochem. 2008 Dec;107(5):1169-87. doi: 10.1111/j.1471-4159.2008.05668.x. Epub 2008 Oct 24.
7
Seizures following picornavirus infection.微小核糖核酸病毒感染后的癫痫发作。
Epilepsia. 2008 Jun;49(6):1066-74. doi: 10.1111/j.1528-1167.2008.01535.x. Epub 2008 Mar 6.
8
Possible role of the innate immunity in temporal lobe epilepsy.先天免疫在颞叶癫痫中的可能作用。
Epilepsia. 2008 Jun;49(6):1055-65. doi: 10.1111/j.1528-1167.2007.01470.x. Epub 2007 Dec 11.
9
Targeting inflammatory demyelinating lesions to sites of Wallerian degeneration.将炎性脱髓鞘病变靶向至华勒氏变性部位。
Am J Pathol. 2007 Nov;171(5):1563-75. doi: 10.2353/ajpath.2007.070147. Epub 2007 Sep 6.
10
Complement activation in experimental and human temporal lobe epilepsy.实验性和人类颞叶癫痫中的补体激活
Neurobiol Dis. 2007 Jun;26(3):497-511. doi: 10.1016/j.nbd.2007.01.015. Epub 2007 Feb 20.

补体在急性病毒感染后癫痫发作发展中的作用。

Role for complement in the development of seizures following acute viral infection.

作者信息

Libbey Jane E, Kirkman Nikki J, Wilcox Karen S, White H Steve, Fujinami Robert S

机构信息

Department of Pathology, University of Utah, 30 North 1900 East, Salt Lake City, UT 84132, USA.

出版信息

J Virol. 2010 Jul;84(13):6452-60. doi: 10.1128/JVI.00422-10. Epub 2010 Apr 28.

DOI:10.1128/JVI.00422-10
PMID:20427530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2903264/
Abstract

Complement, part of the innate immune system, acts to remove pathogens and unwanted host material. Complement is known to function in all tissues, including the central nervous system (CNS). In this study, we demonstrated the importance of the complement system within the CNS in the development of behavioral seizures following Theiler's murine encephalomyelitis virus (TMEV) infection. C57BL/6 mice, deficient in complement component C3, developed significantly fewer behavioral seizures following TMEV infection, whereas mice depleted of complement component C3 in the periphery through treatment with cobra venom factor had a seizure rate comparable to that of control mice. These studies indicate that C3 participates in the induction of acute seizures during viral encephalitis.

摘要

补体作为固有免疫系统的一部分,其作用是清除病原体和不需要的宿主物质。已知补体在包括中枢神经系统(CNS)在内的所有组织中发挥作用。在本研究中,我们证明了中枢神经系统内补体系统在泰勒氏鼠脑脊髓炎病毒(TMEV)感染后行为性癫痫发作发展过程中的重要性。缺乏补体成分C3的C57BL/6小鼠在TMEV感染后发生行为性癫痫发作的次数明显减少,而通过眼镜蛇毒因子处理使外周补体成分C3耗竭的小鼠,其癫痫发作率与对照小鼠相当。这些研究表明,C3参与病毒性脑炎期间急性癫痫发作的诱导。