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T-regulatory cells as part of strategy of immune evasion by pathogens

机译：T调节细胞是病原体免疫逃避策略的一部分

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Under physiological conditions, regulatory processes can suppress the immune response after elimination of a pathogen and restore homeostasis through the destruction and suppression of obsolete effector cells of the immune system. The main players in this process are T-regulatory cells (Tregs) and immature dendritic cells, which suppress the immune response by their own products and/or by inducing synthesis of immunosuppressive interleukins IL-10, IL-35, and transforming growth factor (TGF-) by other cells. This mechanism is also used by widespread "successful" pathogens that are capable of chronically persisting in the human body - herpes virus, hepatitis viruses, human immunodeficiency virus, Mycobacterium tuberculosis, Helicobacter pylori, and others. During coevolution of microbial pathogens and the host immune system, the pathogens developed sophisticated strategies for evading the host defense, so-called immune evasion. In particular, molecular structures of pathogens during the interaction with dendritic cells via activating and inhibitory receptors can change intracellular signal transduction, resulting in block of maturation of dendritic cells. Immature dendritic cells become tolerogenic and cause differentiation of Tregs from the conventional T-cell CD4(+). Microbial molecules can also react directly with Tregs through innate immune receptors. Costimulation of Toll-like receptor 5 (TLR5) by flagellin increases the expression of the transcription factor Foxp3, which increases the suppressive activity of Treg cells. From all evasion mechanisms, the induction of immunosuppression by Treg through IL-10, IL-35, and TGF- appears most effective. This results in the suppression of inflammation and of adaptive immune responses against pathogens, optimizing the conditions for the survival of bacteria and viruses.
机译：在生理条件下，调节过程可以消除病原体后抑制免疫反应，并通过破坏和抑制免疫系统过时的效应细胞来恢复体内平衡。这个过程中的主要参与者是T调节细胞（Tregs）和未成熟的树突状细胞，它们通过自身的产物和/或通过诱导免疫抑制性白介素IL-10，IL-35和转化生长因子的合成来抑制免疫应答。 TGF-）被其他细胞。这种机制还被能够长期存在于人体中的广泛的“成功”病原体所使用，这些病原体包括疱疹病毒，肝炎病毒，人类免疫缺陷病毒，结核分枝杆菌，幽门螺杆菌等。在微生物病原体与宿主免疫系统的共同进化过程中，病原体制定了逃避宿主防御的复杂策略，即所谓的免疫逃避。特别是，病原体的分子结构在通过激活和抑制受体与树突状细胞相互作用的过程中会改变细胞内信号转导，导致树突状细胞的成熟受阻。未成熟的树突状细胞变得耐受，并导致Tregs与常规T细胞CD4（+）分化。微生物分子还可以通过先天免疫受体直接与Tregs反应。鞭毛蛋白对Toll样受体5（TLR5）的共刺激作用会增加转录因子Foxp3的表达，从而增加Treg细胞的抑制活性。从所有逃避机制来看，Treg通过IL-10，IL-35和TGF-诱导免疫抑制似乎最有效。这样可以抑制炎症和针对病原体的适应性免疫反应，从而优化细菌和病毒的生存条件。

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