Helminth parasites infect an alarmingly large proportion of the world's population, primarily within tropical regions, and their ability to down‐modulate host immunity is key to their persistence. Helminths have developed multiple mechanisms that induce a state of hyporesponsiveness or immune suppression within the host; of particular interest are mechanisms that drive the induction of regulatory T‐cells (Tregs). Helminths actively induce Tregs either directly by secreting factors, such as the TGF‐β mimic Hp‐ TGM, or indirectly by interacting with bystander cell types such as dendritic cells and macrophages that then induce Tregs. Expansion of Tregs not only enhances parasite survival but, in cases such as filarial infection, Tregs also play a role in preventing parasite‐associated pathologies. Furthermore, Tregs generated during helminth infection have been associated with suppression of bystander immunopathologies in a range of inflammatory conditions such as allergy and autoimmune disease. In this review, we discuss evidence from natural and experimental infections that point to the pathways and molecules involved in helminth Treg induction, and postulate how parasite‐derived molecules and/or Tregs might be applied as anti‐inflammatory therapies in the future.

中文翻译：

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蠕虫感染中的调节性T细胞：诱导，功能和治疗潜力。

蠕虫寄生虫主要在热带地区感染令人震惊的世界人口比例，其下调宿主免疫力的能力是其持久性的关键。蠕虫已发展出多种机制，可诱导宿主体内反应不足或免疫抑制状态。特别令人感兴趣的是驱动调节性T细胞（Tregs）诱导的机制。蠕虫通过分泌因子（例如TGF-β模拟Hp-）直接主动诱导Treg。TGM，或间接与旁观者细胞类型（例如树突状细胞和巨噬细胞）相互作用，然后诱导Treg。Tregs的扩增不仅可以提高寄生虫的存活率，而且在丝虫感染等情况下，Tregs还可在预防寄生虫相关的疾病中发挥作用。此外，在蠕虫感染期间产生的Treg已与一系列炎症性疾病（如变态反应和自身免疫性疾病）中旁观者免疫病理学的抑制有关。在这篇综述中，我们讨论了来自自然和实验性感染的证据，这些证据指出了蠕虫Treg诱导所涉及的途径和分子，并提出了将来可能将寄生虫衍生的分子和/或Tregs用作抗炎疗法的假设。