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莱姆病:从感染到自身免疫

Lyme borreliosis: from infection to autoimmunity.

作者信息

Singh S K, Girschick H J

机构信息

Paediatric Rheumatology, Children's Hospital, University of Würzburg, Würzburg, Germany.

出版信息

Clin Microbiol Infect. 2004 Jul;10(7):598-614. doi: 10.1111/j.1469-0691.2004.00895.x.

DOI:10.1111/j.1469-0691.2004.00895.x
PMID:15214872
Abstract

Lyme borreliosis in humans is an inflammatory disease affecting multiple organ systems, including the nervous system, cardiovascular system, joints and muscles. The causative agent, the spirochaete Borrelia burgdorferi, is transmitted to the host by a tick bite. The pathogenesis of the disease in its early stages is associated largely with the presence of viable bacteria at the site of inflammation, whereas in the later stages of disease, autoimmune features seem to contribute significantly. In addition, it has been suggested that chronic persistence of B. burgdorferi in affected tissues is of pathogenic relevance. Long-term exposure of the host immune system to spirochaetes and/or borrelial compounds may induce chronic autoimmune disease. The study of bacterium-host interactions has revealed a variety of proinflammatory and also immunomodulatory-immunosuppressive features caused by the pathogen. Therapeutic strategies using antibiotics are generally successful, but chronic disease may require immunosuppressive treatment. Effective and safe vaccines using recombinant outer surface protein A have been developed, but have not been propagated because of fears that autoimmunity might be induced. Nevertheless, new insights into the modes of transmission of B. burgdorferi to the warm-blooded host have been generated by studying the action of these vaccines.

摘要

人类莱姆病是一种影响多个器官系统的炎症性疾病,包括神经系统、心血管系统、关节和肌肉。病原体是螺旋体伯氏疏螺旋体,通过蜱虫叮咬传播给宿主。该疾病早期的发病机制很大程度上与炎症部位存在活细菌有关,而在疾病后期,自身免疫特征似乎起了重要作用。此外,有研究表明伯氏疏螺旋体在受影响组织中的长期持续存在具有致病相关性。宿主免疫系统长期暴露于螺旋体和/或疏螺旋体化合物可能会诱发慢性自身免疫性疾病。对细菌与宿主相互作用的研究揭示了病原体引起的多种促炎以及免疫调节-免疫抑制特征。使用抗生素的治疗策略通常是成功的,但慢性病可能需要免疫抑制治疗。已经开发出使用重组外膜蛋白A的有效且安全的疫苗,但由于担心可能诱发自身免疫而未推广。然而,通过研究这些疫苗的作用,人们对伯氏疏螺旋体向温血宿主的传播方式有了新的认识。

相似文献

1
Lyme borreliosis: from infection to autoimmunity.莱姆病:从感染到自身免疫
Clin Microbiol Infect. 2004 Jul;10(7):598-614. doi: 10.1111/j.1469-0691.2004.00895.x.
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Molecular mimicry to Borrelia burgdorferi: pathway to autoimmunity?对伯氏疏螺旋体的分子模拟:自身免疫之路?
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[New aspects of pathogenesis of Lyme borreliosis].[莱姆病发病机制的新方面]
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Lyme borreliosis (Lyme disease): molecular and cellular pathobiology and prospects for prevention, diagnosis and treatment.莱姆病:分子与细胞病理生物学以及预防、诊断和治疗的前景
Expert Rev Mol Med. 2004 Jan 19;6(2):1-22. doi: 10.1017/S1462399404007276.
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Infection and musculoskeletal conditions: Lyme borreliosis.感染与肌肉骨骼疾病:莱姆病。
Best Pract Res Clin Rheumatol. 2006 Dec;20(6):1099-118. doi: 10.1016/j.berh.2006.08.006.
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Tick-host-pathogen interactions in Lyme borreliosis.莱姆病中蜱-宿主-病原体的相互作用
Trends Parasitol. 2007 Sep;23(9):434-8. doi: 10.1016/j.pt.2007.07.001. Epub 2007 Jul 25.
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Molecular characterization of the OspA(161-175) T cell epitope associated with treatment-resistant Lyme arthritis: differences among the three pathogenic species of Borrelia burgdorferi sensu lato.与难治性莱姆关节炎相关的OspA(161 - 175) T细胞表位的分子特征:狭义伯氏疏螺旋体三种致病物种之间的差异
J Autoimmun. 2004 Nov;23(3):281-92. doi: 10.1016/j.jaut.2004.06.005.
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Hidden in plain sight: Borrelia burgdorferi and the extracellular matrix.隐匿于众目睽睽之下:伯氏疏螺旋体与细胞外基质
Trends Microbiol. 2007 Aug;15(8):350-4. doi: 10.1016/j.tim.2007.06.003. Epub 2007 Jun 27.
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Dermatological manifestations of Lyme borreliosis.莱姆病的皮肤表现
Eur J Dermatol. 2004 Sep-Oct;14(5):296-309.
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[Clinico-pathological collations in borreliosis].[莱姆病的临床病理对照]
Pol Merkur Lekarski. 2006 Jun;20(120):731-4.

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