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有证据表明,莱姆病螺旋体的BBA68蛋白(BbCRASP-1)对人类和其他动物中因子H介导的免疫逃逸没有作用。

Evidence that the BBA68 protein (BbCRASP-1) of the Lyme disease spirochetes does not contribute to factor H-mediated immune evasion in humans and other animals.

作者信息

McDowell John V, Hovis Kelley M, Zhang Hongming, Tran Emily, Lankford Justin, Marconi R T

机构信息

Department of Microbiology and Immunology, Medical College of Virginia at Virginia Commonwealth University, Richmond, VA 23298-0678, USA.

出版信息

Infect Immun. 2006 May;74(5):3030-4. doi: 10.1128/IAI.74.5.3030-3034.2006.

DOI:10.1128/IAI.74.5.3030-3034.2006
PMID:16622245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1459725/
Abstract

BBA68 (BbCRASP-1) of the Lyme disease spirochetes binds human factor H (FH) and FH-like protein 1 (FHL-1). Here we assess transcription of the BBA68 gene and production of BBA68 in infected mice and humans using real-time reverse transcriptase PCR and immunoblotting. The species specificity of FH binding to BBA68 was also tested. The data suggest that BBA68 does not play an important role in immune evasion in animals.

摘要

莱姆病螺旋体的BBA68(BbCRASP-1)可结合人补体因子H(FH)和类补体因子H蛋白1(FHL-1)。在此,我们运用实时逆转录聚合酶链反应和免疫印迹法评估了BBA68基因在受感染小鼠和人类中的转录情况以及BBA68的产生。同时还检测了FH与BBA68结合的物种特异性。数据表明,BBA68在动物的免疫逃逸中并不起重要作用。

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本文引用的文献

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Selective binding of Borrelia burgdorferi OspE paralogs to factor H and serum proteins from diverse animals: possible expansion of the role of OspE in Lyme disease pathogenesis.伯氏疏螺旋体OspE旁系同源物与不同动物的补体因子H和血清蛋白的选择性结合:OspE在莱姆病发病机制中作用的可能扩展
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Demonstration of OspC type diversity in invasive human lyme disease isolates and identification of previously uncharacterized epitopes that define the specificity of the OspC murine antibody response.侵袭性人类莱姆病分离株中OspC类型多样性的展示以及对定义OspC鼠抗体反应特异性的先前未表征表位的鉴定。
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Demonstration of cotranscription and 1-methyl-3-nitroso-nitroguanidine induction of a 30-gene operon of Borrelia burgdorferi: evidence that the 32-kilobase circular plasmids are prophages.伯氏疏螺旋体30基因操纵子的共转录及1-甲基-3-亚硝基胍诱导的证明:32千碱基环状质粒是原噬菌体的证据
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Borrelia burgdorferi regulates expression of complement regulator-acquiring surface protein 1 during the mammal-tick infection cycle.伯氏疏螺旋体在哺乳动物-蜱虫感染周期中调控补体调节蛋白获取表面蛋白1的表达。
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Demonstration of factor H-like protein 1 binding to Treponema denticola, a pathogen associated with periodontal disease in humans.证明类补体因子H1蛋白与齿垢密螺旋体结合,齿垢密螺旋体是一种与人类牙周疾病相关的病原体。
Infect Immun. 2005 Nov;73(11):7126-32. doi: 10.1128/IAI.73.11.7126-7132.2005.
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Complement regulator-acquiring surface protein 1 imparts resistance to human serum in Borrelia burgdorferi.补体调节蛋白获取表面蛋白1赋予伯氏疏螺旋体对人血清的抗性。
J Immunol. 2005 Sep 1;175(5):3299-308. doi: 10.4049/jimmunol.175.5.3299.
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Human Lyme arthritis and the immunoglobulin G antibody response to the 37-kilodalton arthritis-related protein of Borrelia burgdorferi.人类莱姆关节炎以及针对伯氏疏螺旋体37千道尔顿关节炎相关蛋白的免疫球蛋白G抗体反应。
Infect Immun. 2005 May;73(5):2951-7. doi: 10.1128/IAI.73.5.2951-2957.2005.
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Infect Immun. 2005 Apr;73(4):2351-9. doi: 10.1128/IAI.73.4.2351-2359.2005.
9
Putative coiled-coil structural elements of the BBA68 protein of Lyme disease spirochetes are required for formation of its factor H binding site.莱姆病螺旋体的BBA68蛋白的假定卷曲螺旋结构元件是其因子H结合位点形成所必需的。
J Bacteriol. 2005 Feb;187(4):1317-23. doi: 10.1128/JB.187.4.1317-1323.2005.
10
RpoS is not central to the general stress response in Borrelia burgdorferi but does control expression of one or more essential virulence determinants.RpoS对伯氏疏螺旋体的一般应激反应并非至关重要,但它确实控制着一种或多种关键毒力决定因素的表达。
Infect Immun. 2004 Nov;72(11):6433-45. doi: 10.1128/IAI.72.11.6433-6445.2004.