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恰加斯病的发病机制:是时候取得进展了。

Pathogenesis of Chagas disease: time to move on.

作者信息

Machado Fabiana S, Tyler Kevin M, Brant Fatima, Esper Lisia, Teixeira Mauro M, Tanowitz Herbert B

机构信息

Department of Biochemistry and Immunology, Institute of Biological Sciences, Belo Horizonte, Brazil.

出版信息

Front Biosci (Elite Ed). 2012 Jan 1;4(5):1743-58. doi: 10.2741/495.

DOI:10.2741/495
PMID:22201990
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3255071/
Abstract

Trypanosoma cruzi is the etiologic agent of Chagas disease. The contributions of parasite and immune system for disease pathogenesis remain unresolved and controversial. The possibility that Chagas disease was an autoimmune progression triggered by T. cruzi infection led some to question the benefit of treating chronically T. cruzi-infected persons with drugs. Furthermore, it provided the rationale for not investing in research aimed at a vaccine which might carry a risk of inducing autoimmunity or exacerbating inflammation. This viewpoint was adopted by cash-strapped health systems in the developing economies where the disease is endemic and has been repeatedly challenged by researchers and clinicians in recent years and there is now a considerable body of evidence and broad consensus that parasite persistence is requisite for pathogenesis and that antiparasitic immunity can be protective against T. cruzi pathogenesis without eliciting autoimmune pathology. Thus, treatment of chronically infected patients is likely to yield positive outcomes and efforts to understand immunity and vaccine development should be recognized as a priority area of research for Chagas disease.

摘要

克氏锥虫是恰加斯病的病原体。寄生虫和免疫系统在疾病发病机制中的作用仍未得到解决且存在争议。恰加斯病是由克氏锥虫感染引发的自身免疫进展这一可能性,导致一些人质疑用药物治疗慢性克氏锥虫感染患者的益处。此外,这也为不投资于可能存在诱导自身免疫或加剧炎症风险的疫苗研究提供了理论依据。这种观点被疾病流行的发展中经济体资金紧张的卫生系统所采纳,近年来研究人员和临床医生对此提出了反复质疑,现在有大量证据和广泛共识表明,寄生虫持续存在是发病机制所必需的,并且抗寄生虫免疫可以预防克氏锥虫发病机制而不引发自身免疫病理。因此,治疗慢性感染患者可能会产生积极结果,并且理解免疫和疫苗开发的努力应被视为恰加斯病研究的优先领域。

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本文引用的文献

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Heat-killed Trypanosoma cruzi induces acute cardiac damage and polyantigenic autoimmunity.加热杀死的克氏锥虫诱导急性心脏损伤和多抗原自身免疫。
PLoS One. 2011 Jan 21;6(1):e14571. doi: 10.1371/journal.pone.0014571.
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In vivo infection by Trypanosoma cruzi: the conserved FLY domain of the gp85/trans-sialidase family potentiates host infection.克氏锥虫体内感染:gp85/转涎酶家族的保守 FLY 结构域增强了宿主感染。
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Myocardial gene and protein expression profiles after autoimmune injury in Chagas' disease cardiomyopathy.自身免疫性损伤后克山病心肌病的心肌基因和蛋白质表达谱。
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Chagas disease: changes in knowledge and management.恰加斯病:知识和管理的变化。
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IL-17 is necessary for host protection against acute-phase Trypanosoma cruzi infection.IL-17 对于宿主抵抗急性期克氏锥虫感染是必需的。
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IL-17 produced during Trypanosoma cruzi infection plays a central role in regulating parasite-induced myocarditis.在克氏锥虫感染过程中产生的白细胞介素 17 在调节寄生虫引起的心肌炎中起着核心作用。
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The role of parasite persistence in pathogenesis of Chagas heart disease.寄生虫持续存在在恰加斯心脏病发病机制中的作用。
Parasite Immunol. 2009 Nov;31(11):673-85. doi: 10.1111/j.1365-3024.2009.01108.x.
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