Abnormal expression of CD96 on natural killer cell in peripheral blood of patients with chronic obstructive pulmonary disease

• Published in: The clinical respiratory journal Vol. 16; no. 8; pp. 546 - 554
• Main Authors: Zhao, Xiaomin, Feng, Xiaowen, Liu, Pengcheng, Ye, Jing, Tao, Rui, Li, Renming, Shen, Bing, Zhang, Xiaoming, Wang, Xuefu, Zhao, Dahai
• Format: Journal Article
• Language: English
• Published: Copenhagen John Wiley & Sons, Inc 01.08.2022; John Wiley and Sons Inc; Wiley
• Subjects: Antibodies; CD16; CD96; Chronic obstructive pulmonary disease; COPD; Flow cytometry; Gene expression; LUNG; NK cell; Original
• ISSN: 1752-6981; 1752-699X
• DOI: 10.1111/crj.13523

Natural killer (NK) cells are regarded as the host's first line of defense against viral infection. Moreover, the involvement of NK cells in chronic obstructive pulmonary disease (COPD) has been documented. However, the specific mechanism and biological changes of NK cells in COPD development have not been determined. In this study, we extracted NK cells from the peripheral blood of 18 COPD patients who were recovering from an acute exacerbation and 45 healthy donors (HDs), then we labeled NK cells with different antibodies and analyzed with flow cytometry. The data showed that the frequencies of total NK cells in the peripheral blood of COPD patients were lower compared with HDs. Moreover, the inhibitory receptors on NK cells expressed higher levels and the expression of activating receptors were generally low. Importantly, both the expression levels of CD96 in NK cells and the frequencies of CD96+ NK cells were significantly upregulated in COPD patients. These findings suggest that surface receptor CD96 from NK cells may be a risk factor in the evolution of COPD. The study shows that the expression levels of NK cell surface receptors were abnormal in chronic obstructive pulmonary disease (COPD) patients compared with healthy controls, especially inhibitory receptors CD96. These findings suggest that surface receptor CD96 from NK cells may be a risk factor in the evolution of COPD.