Regulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination.

Regulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination.
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在传染病和疫苗接种中,人类宿主与病原体之间的界面的调节性T细胞。

DOI:
10.3389/fimmu.2015.00217
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发表时间:
2015
影响因子:
7.3
通讯作者:
Ottenhoff TH
Ottenhoff TH
中科院分区:
医学2区
文献类型:
--
作者:
Boer MC;Joosten SA;Ottenhoff TH

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调节性T细胞(Tcells)在人类感染性疾病中作用于宿主和病原体相互作用的界面。结核病是由多种病原体引起的,但结核病对不同病原体和感染的不同阶段有不同的作用。此外,由特定病原体诱导的T细胞可以非特异性地抑制针对其他微生物和寄生虫的免疫。因此,Treg效应不仅需要在同源中评估,而且需要在异源感染和疫苗接种中评估。虽然THBE保护人类宿主免受过度炎症,但它们也可能增加病原体持续存在和慢性疾病的风险,以及疾病在生命后期重新激活的可能性。麻风分枝杆菌和结核分枝杆菌,分别引起麻风病和结核病,是人类已知的最古老的微生物之一,是免疫系统对耐受性和病原体持久性的主要操纵者。大多数分枝杆菌感染发生在病毒、寄生虫和(其他)细菌合并感染共同流行的环境中。在本文中,我们讨论了最近的见解在人类感染性疾病中的活化和活性的THBE,重点是早期,晚期和疾病,合并感染和疫苗接种的非特异性影响。我们强调分枝杆菌感染的重要模式的调制主机的反应和疫苗诱导的免疫力的Teptide。
Regulatory T-cells (Tregs) act at the interface of host and pathogen interactions in human infectious diseases. Tregs are induced by a wide range of pathogens, but distinct effects of Tregs have been demonstrated for different pathogens and in different stages of infection. Moreover, Tregs that are induced by a specific pathogen may non-specifically suppress immunity against other microbes and parasites. Thus, Treg effects need to be assessed not only in homologous but also in heterologous infections and vaccinations. Though Tregs protect the human host against excessive inflammation, they probably also increase the risk of pathogen persistence and chronic disease, and the possibility of disease reactivation later in life. Mycobacterium leprae and Mycobacterium tuberculosis, causing leprosy and tuberculosis, respectively, are among the most ancient microbes known to mankind, and are master manipulators of the immune system toward tolerance and pathogen persistence. The majority of mycobacterial infections occur in settings co-endemic for viral, parasitic, and (other) bacterial coinfections. In this paper, we discuss recent insights in the activation and activity of Tregs in human infectious diseases, with emphasis on early, late, and non-specific effects in disease, coinfections, and vaccination. We highlight mycobacterial infections as important models of modulation of host responses and vaccine-induced immunity by Tregs.
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