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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Foxp3 + regulatory T cells, immune stimulation and host defence against infection
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Foxp3 + regulatory T cells, immune stimulation and host defence against infection

机译：Foxp3 +调节性T细胞，免疫刺激和宿主防御感染

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The immune system is intricately regulated allowing potent effectors to expand and become rapidly mobilized after infection, while simultaneously silencing potentially detrimental responses that averts immune-mediated damage to host tissues. This relies in large part on the delicate interplay between immune suppressive regulatory CD4 + T (Treg) cells and immune effectors that without active suppression by Treg cells cause systemic and organ-specific autoimmunity. Although these beneficial roles have been classically described as counterbalanced by impaired host defence against infection, newfound protective roles for Treg cells against specific viral pathogens (e.g. herpes simplex virus 2, lymphocytic choriomeningitis virus, West Nile virus) have been uncovered using transgenic mice that allow in vivo Treg-cell ablation based on Foxp3 expression. In turn, Foxp3 + Treg cells also provide protection against some parasitic (Plasmodium sp., Toxoplasma gondii) and fungal (Candida albicans) pathogens. By contrast, for bacterial and mycobacterial infections (e.g. Listeria monocytogenes, Salmonella enterica, Mycobacterium tuberculosis), experimental manipulation of Foxp3 + cells continues to indicate detrimental roles for Treg cells in host defence. This variance is probably related to functional plasticity in Treg cell suppression that shifts discordantly following infection with different types of pathogens. Furthermore, the efficiency whereby Treg cells silence immune activation coupled with the plasticity in Foxp3 + cell activity suggest that overriding Treg-mediated suppression represents a prerequisite 'signal zero' that together with other stimulation signals [T-cell receptor (signal 1), co-stimulation (signal 2), inflammatory cytokines (signal 3)] are essential for T-cell activation in vivo. Herein, the importance of Foxp3 + Treg cells in host defence against infection, and the significance of infection-induced shifts in Treg-cell suppression are summarized.
机译：免疫系统经过复杂的调节，可以使强大的效应子在感染后扩展并迅速动员，同时沉默潜在的有害反应，从而避免免疫介导的对宿主组织的损害。这在很大程度上取决于免疫抑制性调节性CD4 + T（Treg）细胞与免疫效应物之间的微妙相互作用，这种相互作用在没有Treg细胞主动抑制的情况下会引起全身性和器官特异性自身免疫。尽管经典地描述了这些有益作用是通过抵抗宿主对感染的防御作用来抵消的，但已经发现转基因小鼠对Treg细胞抵抗特定病毒病原体（例如单纯疱疹病毒2，淋巴细胞性脉络膜脑膜炎病毒，西尼罗河病毒）具有新的保护作用。 Foxp3表达的体内Treg细胞消融。反过来，Foxp3 + Treg细胞也可提供针对某些寄生虫（疟原虫，弓形虫）和真菌（白色念珠菌）病原体的保护。相比之下，对于细菌和分枝杆菌感染（例如单核细胞增生李斯特菌，肠炎沙门氏菌，结核分枝杆菌），Foxp3 +细胞的实验操作继续表明Treg细胞在宿主防御中具有有害作用。这种差异可能与Treg细胞抑制中的功能可塑性有关，后者在感染不同类型的病原体后会发生不一致的变化。此外，Treg细胞沉默免疫激活以及Foxp3 +细胞活性可塑性的效率表明，超越Treg介导的抑制作用是先决条件“信号零”，它与其他刺激信号[T细胞受体（信号1），共同-刺激（信号2），炎性细胞因子（信号3）]对于体内T细胞活化至关重要。本文总结了Foxp3 + Treg细胞在宿主抵抗感染中的重要性，以及感染诱导的Treg细胞抑制转移的重要性。

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