Disrupted balance of CD4+ T-cell subsets in bone marrow of patients with primary immune thrombocytopenia
Disrupted balance of CD4+ T-cell subsets in bone marrow of patients with primary immune thrombocytopenia
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原发性免疫性血小板减少症患者骨髓中 CD4( ) T 细胞亚群的平衡被破坏
DOI：
10.7150/ijbs.33779
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发表时间：
2019-01-01
影响因子：
9.2
通讯作者：
Liu, Xin-guang
中科院分区：
文献类型：
--
作者：
Wang, Qian;Li, Juan;Liu, Xin-guang
原发性免疫性血小板减少症（ITP）患者外周血（PB）中CD4(+) t细胞亚群的不平衡已经得到了很好的证实，而骨髓（BM）中CD4(+) t细胞亚群的分布仍然难以捉摸。本研究测定了活动性ITP患者和健康对照（hc） BM和PB中辅助性T细胞22 （Th22）、Th17、Th1、Th2、滤泡性T细胞（Tfh）和调节性T细胞（Tregs）及其效应细胞因子的频率。结果显示，ITP患者BM中Th22、Th17、Th1和Tfh细胞的频率显著高于hcc，而Treg细胞的数量显著低于hcc。在ITP组中，BM中Th22、Th17、Th1、Th2和Tfh细胞的数量明显高于与之匹配的PB组，而BM中的Treg细胞数量明显低于PB组。与HCs患者相比，ITP患者BM的血浆白细胞介素(IL)-22、IL- 17a和干扰素(INF)- γ水平显著升高，这与BM Th亚群模式一致。因此，在ITP患者的BM和PB中，CD4(+) t细胞亚群的平衡被破坏，提示这可能在ITP的病理生理过程中起重要作用。
Disequilibrium of CD4(+) T-cell subpopulations in peripheral blood (PB) of patients with primary immune thrombocytopenia (ITP) has been well established, whereas the profile of CD4(+) T-cell subpopulations in bone marrow (BM) remains elusive. In the present study, the frequencies of T helper 22 (Th22), Th17, Th1, Th2, follicular T helper (Tfh) cells and regulatory T cells (Tregs) as well as their effector cytokines in BM and PB from active ITP patients and healthy controls (HCs) were determined. Results showed that the frequencies of Th22, Th17, Th1, and Tfh cells were significantly higher, but Treg number was remarkably lower in BM from ITP patients than from HCs. In the ITP group, it was notable that the numbers of BM Th22, Th17, Th1, Th2, and Tfh cells were significantly elevated compared with the matched PB counterparts, while Treg number in BM was considerably reduced compared with that in PB. In consistence with the BM Th subset pattern, plasma levels of interleukin (IL)-22, IL-17A, and interferon (INF)-gamma in BM from ITP patients were significantly increased compared with that from HCs. Therefore, the balance of CD4(+) T-cell subsets was disrupted in both BM and PB of ITP patients, suggesting that this might play important roles in the pathophysiological process of ITP.