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To be or not to be: CD25 expression by regulatory CD4+ T cells in the prevention of allergic inflammation.

机译:成为或不成为:CD25通过调节CD4 + T细胞在预防过敏性炎症中的表达。

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摘要

The study of CD4~+ T cells with a 'regulatory' or 'suppres-sive' capacity has a chequered history, with seminal rodent studies in this area on autoimmune disease and transplantation tolerance dating back to the 1980s [1, 2]. Unfortunately, the importance of these early studies was not fully grasped at the time, mainly due to the fact that a reliable marker was not available that could distinguish regulatory and effector populations of CD4~+ T cells. Candidate markers including CD 2 5 and isoforms of CD45 were identified in these early studies [1, 2]; however, it was not until the mid-1990s that the field would change dramatically: studies in mice started to emerge from the Sakaguchi laboratory that confirmed CD25 as a functional marker that could identify what now are known as CD4~+ CD25~+ T regulatory (Treg) cells that could prevent organ specific autoimmunity [3]
机译:CD4〜+ T细胞的研究具有“监管”或“Suppres-and”的能力,具有格仔的历史,在这一领域具有精心免疫疾病和移植耐受的初始啮齿动物研究,可追溯到20世纪80年代[1,2]。 遗憾的是,当时,这些早期研究的重要性并未完全掌握,主要是由于无法区分CD4〜+ T细胞的调节和效应群体的可靠标记。 在这些早期研究中鉴定了包括CD 2 5和CD45同种型的候选标志物[1,2]; 然而,直到20世纪90年代中期,该领域将急剧变化:小鼠的研究开始从Sakaguchi实验室开始,该实验室证实了CD25作为功能标记,可以确定现在称为CD4〜+ CD25〜+ T调节 (Treg)可以预防器官特异性自身免疫的细胞[3]

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