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Regulatory T cells suppress antigen-driven CD4 T cell reactivity following injury

机译:调节性T细胞在损伤后抑制抗原驱动的CD4 T细胞反应性

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摘要

Injury initiates local and systemic host responses and is known to increase CD4 Treg activity in mice and humans. This study uses a TCR transgenic T cell adoptive transfer approach and in vivo Treg depletion to determine specifically the in vivo influence of Tregs on antigen-driven CD4 T cell reactivity following burn injury in mice. We report here that injury in the absence of recipient and donor Tregs promotes high antigen-driven CD4 T cell expansion and increases the level of CD4 T cell reactivity. In contrast, CD4 T cell expansion and reactivity were suppressed significantly in injured Treg-replete mice. In additional experiments, we found that APCs prepared from burn- or sham-injured, Treg-depleted mice displayed significantly higher antigen-presenting activity than APCs prepared from normal mice, suggesting that Tregs may suppress injury responses by controlling the intensity of APC activity. Taken together, these findings demonstrate that Tregs can actively control the in vivo expansion and reactivity of antigen-stimulated, naïve CD4 T cells following severe injury.
机译:损伤会引发局部和全身宿主反应,已知会增加小鼠和人类的CD4 Treg活性。这项研究使用TCR转基因T细胞过继转移方法和体内Treg耗竭来具体确定Treg对小鼠烧伤后抗原驱动的CD4 T细胞反应性的体内影响。我们在这里报告说,在没有受体和供体Tregs的情况下的损伤会促进高抗原驱动的CD4 T细胞扩增并增加CD4 T细胞反应性的水平。相反,在受伤的Treg充足的小鼠中,CD4T细胞的扩增和反应性被显着抑制。在其他实验中,我们发现用烧伤或假伤的Treg耗竭小鼠制备的APC的抗原呈递活性明显高于用正常小鼠制备的APC,这表明Tregs可通过控制APC活性的强度来抑制损伤反应。综上所述,这些发现表明,Tregs可以在严重损伤后主动控制抗原刺激的幼稚CD4 T细胞的体内扩增和反应性。

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