Forkhead box P3 (FOXP3)+ regulatory T cell (Treg) reconstitution after unrelated donor umbilical cord blood transplantation in chemotherapy-naïve children is incompletely characterized. We studied 21 children with nonmalignant diseases receiving an identical alemtuzumab-containing regimen. We hypothesized that Treg recovery may be perturbed in patients not only by acute graft-versus-host disease (aGVHD) but also by viremia. Tregs and their memory and naïve subsets were serially monitored for proliferation and apoptosis along with conventional T cells (Tcon). A "reconstitution index" (RI) was calculated relative to pretransplantation values for each parameter. At 3 months post-UCBT, the RI of Tregs was faster compared with other immune components tested and was most rapid in patients free of aGVHD and viremia. There were significantly fewer Tregs in patients experiencing grade I-II aGVHD and/or viremia, leading to an imbalance between Tregs-Tcon ratios. Central and effector memory Tregs were most affected at this time point when they dominated in the circulation. Impaired Treg proliferation without increased apoptosis accounted for the reduced Treg-Tcon ratio. In patients affected with grade II aGVHD and viremia, the overall reduction in circulating Treg pool were associated with a more oligoclonal T-cell receptor β repertoire. Taken together, aGVHD and viremia can lead to defective Treg expansion homeostasis.

中文翻译：

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调节性 T 细胞亚群的快速重建与使用阿仑单抗进行低强度调节的儿童脐血移植后急性移植物抗宿主病的发生率降低和病毒血症的发生率降低有关

未接受过化疗的儿童在无关供体脐带血移植后的叉头盒 P3 (FOXP3)+ 调节性 T 细胞 (Treg) 重建尚未完全表征。我们研究了 21 名接受相同阿仑单抗治疗方案的非恶性疾病儿童。我们假设患者的 Treg 恢复可能不仅受到急性移植物抗宿主病 (aGVHD) 的干扰，还受到病毒血症的干扰。与常规 T 细胞 (Tcon) 一起，连续监测 Treg 及其记忆和幼稚亚群的增殖和凋亡。相对于每个参数的移植前值计算“重建指数”(RI)。在 UCBT 后 3 个月，Tregs 的 RI 比测试的其他免疫成分更快，并且在没有 aGVHD 和病毒血症的患者中最快。在经历 I-II 级 aGVHD 和/或病毒血症的患者中，Tregs 显着减少，导致 Tregs-Tcon 比率之间的不平衡。中枢和效应记忆 Treg 在这个时间点受到的影响最大，因为它们在循环中占主导地位。Treg 增殖受损而不增加细胞凋亡是 Treg-Tcon 比率降低的原因。在患有 II 级 aGVHD 和病毒血症的患者中，循环 Treg 池的总体减少与更多的寡克隆 T 细胞受体 β 库有关。总之，aGVHD 和病毒血症可导致 Treg 扩增稳态缺陷。Treg 增殖受损而不增加细胞凋亡是 Treg-Tcon 比率降低的原因。在患有 II 级 aGVHD 和病毒血症的患者中，循环 Treg 池的总体减少与更多的寡克隆 T 细胞受体 β 库有关。总之，aGVHD 和病毒血症可导致 Treg 扩增稳态缺陷。Treg 增殖受损而不增加细胞凋亡是 Treg-Tcon 比率降低的原因。在患有 II 级 aGVHD 和病毒血症的患者中，循环 Treg 池的总体减少与更多的寡克隆 T 细胞受体 β 库有关。总之，aGVHD 和病毒血症可导致 Treg 扩增稳态缺陷。