Imbalance between subsets of CD8+ peripheral blood T cells in patients with chronic obstructive pulmonary disease

被引:11
作者
Chen, Long [1 ]
Chen, Gang [1 ]
Zhang, Ming-Qiang [1 ,2 ]
Xiong, Xian-Zhi [1 ]
Liu, Hong-Ju [1 ]
Xin, Jian-Bao [1 ]
Zhang, Jian-Chu [1 ]
Wu, Jiang-Hua [1 ]
Meng, Zhao-Ji [1 ]
Sun, Sheng-Wen [1 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Resp Med, Wuhan, Peoples R China
[2] Tsinghua Univ, Beijing Tsinghua Changgung Hosp, Med Ctr, Dept Resp Med, Beijing, Peoples R China
来源
PEERJ | 2016年 / 4卷
基金
中国国家自然科学基金;
关键词
Cytotoxic T cells; Inflammation; Clinical immunology; Regulatory T cells; NICOTINIC ACETYLCHOLINE-RECEPTOR; SMOKERS; INFLAMMATION; LYMPHOCYTES; COPD; MICE;
D O I
10.7717/peerj.2301
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 (cytutuxic T cells, To 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(+)alpha 7(+) 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. Tcl 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.
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页数:14
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