Disrupting or harnessing immune suppression is leading to new therapeutic avenues in a number of immune‐related diseases. Understanding the suppressive functions of regulatory T cells (Tregs) in different environments is therefore key. Parasitic worms are strong inducers of Tregs and previous research has suggested that parasite‐induced Tregs are stronger suppressors than naïve Tregs. In strains susceptible to the intestinal worm Heligmosomoides polygyrus , like C57BL/6 mice, it has been hypothesized that increased Treg suppression downregulates both Th1 and Th2 responses, leading to chronic infections and high worm burden. Here, we show that the suppressive capacity of Tregs is no different between cells from infected and/or naive animals. In vitro suppression induced by CD4⁺CD25⁺Tregs (Peyers’ Patches or the mesenteric lymph nodes), isolated early (day 7, tissue dwelling phase) or late (day 21, luminal phase) during infection was similar to that induced by cells from naïve animals. Suppression was CTLA‐4 dependent in Tregs from acute but not chronic infection or in Tregs from naïve animals. This highlights the versatility of Tregs and the importance of extensive Treg characterization prior to potential in vivo manipulation of this cell type.

中文翻译：

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Heligmosomoides polygyrus诱导的Treg在C57BL / 6小鼠中的抑制机制随时间而变化，并且与幼稚小鼠不同。

破坏或利用免疫抑制正在导致许多免疫相关疾病的新治疗途径。因此，了解不同环境中调节性T细胞（Tregs）的抑制功能至关重要。寄生虫是Tregs的强力诱因，而先前的研究表明，寄生虫诱导的Tregs比幼稚Tregs更强。像C57BL / 6小鼠一样，在对肠道蠕虫多性拟螺旋体敏感的菌株中，已经假设增加的Treg抑制作用会下调Th1和Th2反应，从而导致慢性感染和高蠕虫负担。在这里，我们表明感染动物和/或幼稚动物的细胞之间Tregs的抑制能力没有区别。CD4 ⁺ CD25诱导的体外抑制⁺ Tregs（派伊尔氏淋巴结或肠系膜淋巴结）在感染过程中的早期（第7天，组织驻留阶段）或晚期（第21天，腔期）分离，与幼稚动物的细胞诱导的Tregs相似。急性感染而非长期感染的Treg或幼稚动物的Treg的抑制作用均依赖于CTLA-4。这突出了Tregs的多功能性以及广泛的Treg特征化在潜在体内操纵这种细胞类型之前的重要性。