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Exemplifying complexity of immune suppression by a "canonical" speech: A glimpse into TNFRSF-activated signaling pathways in Treg cells.
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-05-19 , DOI: 10.1002/eji.202048711 Emira Ayroldi 1 , Ursula Grohmann 2
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-05-19 , DOI: 10.1002/eji.202048711 Emira Ayroldi 1 , Ursula Grohmann 2
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Regulatory T (Treg) cells are crucial mediators of immune tolerance suppressing self‐reactive T cells and preventing autoimmune diseases. Besides activation of the T cell receptor (TCR), empowerment of Treg cell functions requires co‐accessory signals, such as those released by the TNF receptor superfamily (TNFRSF) that, however, can also promote immunostimulatory responses when engaged by effector T cells. In this issue of European Journal of Immunology , Lubrano di Ricco et al. [Eur. J. Immunol. 2020. 50: 972–985] have taken a closer look at the important question of the functional meaning of TNFRSF‐activated signaling pathways in Treg cells. They have demonstrated that costimulation by TNFR2, 4‐1BB, GITR, DR3, but not OX40 in mouse Foxp3+ Treg cells activates the same and unique signaling pathway, i.e., canonical NF‐κB, which in turn leads to Foxp3 gene upregulation, cell expansion in vitro and in vivo, and suppressive activity in an experimental model of colitis. Moreover, induction of markers of T helper 2 (Th2) and Th17 as well as of genes encoding proteins involved in noncanonical NF‐κΒ was also observed. We here discussed how these findings further highlight the emerging concept of Treg cell plasticity in immune tolerance.
中文翻译：
通过“规范”语音举例说明免疫抑制的复杂性：瞥见Treg细胞中TNFRSF激活的信号通路。
调节性T（Treg）细胞是免疫耐受的关键介质，可抑制自身反应性T细胞并预防自身免疫性疾病。除了激活T细胞受体（TCR）外，赋予Treg细胞功能还需要共辅信号，例如TNF受体超家族（TNFRSF）释放的信号，但是，当效应T细胞参与时，它们也可以促进免疫刺激反应。在本期《欧洲免疫学杂志》上，Lubrano di Ricco等人。[欧元。J.免疫。2020. 50：972–985]仔细研究了Treg细胞中TNFRSF激活的信号通路功能意义的重要问题。他们已经证明，TNFR2、4-1BB，GITR，DR3共同刺激小鼠Foxp3 +Treg细胞激活相同且独特的信号传导途径，即经典的NF-κB，进而导致Foxp3基因上调，体内外细胞扩增以及在结肠炎实验模型中的抑制活性。此外，还观察到诱导了T辅助2（Th2）和Th17的标记以及编码非经典NF-κΒ的蛋白质的基因。在这里，我们讨论了这些发现如何进一步突出免疫耐受中Treg细胞可塑性的新兴概念。
更新日期：2020-07-03
中文翻译：
通过“规范”语音举例说明免疫抑制的复杂性：瞥见Treg细胞中TNFRSF激活的信号通路。
调节性T（Treg）细胞是免疫耐受的关键介质，可抑制自身反应性T细胞并预防自身免疫性疾病。除了激活T细胞受体（TCR）外，赋予Treg细胞功能还需要共辅信号，例如TNF受体超家族（TNFRSF）释放的信号，但是，当效应T细胞参与时，它们也可以促进免疫刺激反应。在本期《欧洲免疫学杂志》上，Lubrano di Ricco等人。[欧元。J.免疫。2020. 50：972–985]仔细研究了Treg细胞中TNFRSF激活的信号通路功能意义的重要问题。他们已经证明，TNFR2、4-1BB，GITR，DR3共同刺激小鼠Foxp3 +Treg细胞激活相同且独特的信号传导途径，即经典的NF-κB，进而导致Foxp3基因上调，体内外细胞扩增以及在结肠炎实验模型中的抑制活性。此外，还观察到诱导了T辅助2（Th2）和Th17的标记以及编码非经典NF-κΒ的蛋白质的基因。在这里，我们讨论了这些发现如何进一步突出免疫耐受中Treg细胞可塑性的新兴概念。
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