Imbalance between subsets of CD8(+) peripheral blood T cells in patients with chronic obstructive pulmonary disease.
Imbalance between subsets of CD8(+) peripheral blood T cells in patients with chronic obstructive pulmonary disease.
复制标题
慢性阻塞性肺疾病患者外周血CD8(+)T细胞亚群失衡
作者：
Chen L;Chen G;Zhang MQ;Xiong XZ;Liu HJ;Xin JB;Zhang JC;Wu JH;Meng ZJ;Sun SW
背景已知CD 8 + T淋巴细胞在慢性阻塞性肺疾病（COPD）的发病机制中起关键作用。然而，COPD患者的CD 8 + T细胞（细胞毒性T细胞，Tc）亚群的系统分析尚未得到很好的进行。方法.采用流式细胞术检测24例稳定期COPD患者（SCOPD）、14例急性加重期COPD患者（AECOPD）和14例健康非吸烟者（HN）外周血中Tc 1/2/10/17、CD 8+调节性T细胞（TcR）和CD 8 +α7+ T细胞。结果COPD急性加重伴有循环CD 8 + T细胞水平升高。Tc 1细胞在SCOPD和AECOPD患者中均增加，而Tc 2细胞在SCOPD患者中减少，但在AECOPD患者中保持正常。Tc 17细胞仅在AECOPD患者中增加，而Tc 10细胞的百分比在SCOPD和AECOPD患者中均减少。在COPD中观察到的促炎/抗炎Tc亚群的失衡可能是由Tc 10细胞的缺乏和CD 8 + Tc 10的抗炎能力受损引起的。结论. CD 8 + T细胞亚群失衡是COPD发病机制中免疫应答功能紊乱的重要原因。
Background. CD8+ T lymphocytes are known to play a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, systematic analyses of CD8+ T cell (Cytotoxic T cells, Tc) subsets in COPD patients have yet to be well conducted. Methods. The whole Tc subsets, including Tc1/2/10/17, CD8+ regulatory T cells (Tregs) and CD8+α7+ T cells, were quantified by flow cytometry in peripheral blood from 24 stable COPD subjects (SCOPD), 14 patients during acute exacerbations (AECOPD), and 14 healthy nonsmokers (HN). Results. Acute exacerbations of COPD were accompanied by elevated levels of circulating CD8+ T cells. Tc1 cells were increased in both SCOPD and AECOPD patients, whereas the percentage of Tc2 cells was decreased in SCOPD patients but remained normal in AECOPD patients. Tc17 cells were increased only in AECOPD patients, and the percentage of Tc10 cells was reduced in both SCOPD and AECOPD patients. The imbalances of pro/anti-inflammatory Tc subsets observed in COPD may be caused by the lack of Tc10 cells and the impaired anti-inflammatory capacity of CD8+ Tregs. Conclusions. The imbalances between subsets of CD8+ peripheral blood T cells contribute to the immune response dysfunction in COPD pathogenesis.