Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Road, Wuhan, 430030, China.
Respir Res. 2020 Mar 11;21(1):66. doi: 10.1186/s12931-020-01333-z.
It has been reported that B cell activating factor belonging to the tumor necrosis factor family (BAFF) expression is increased in chronic obstructive pulmonary disease (COPD). However its role in this chronic inflammatory disease is not fully understood. Previous studies have suggested that BAFF also affects T cell function. We therefore investigated the effects of BAFF on T lymphocytes in COPD.
BAFF was detected in the cells of sputum and the plasma. Peripheral blood mononuclear cells (PBMCs) were isolated from COPD patients and treated with BAFF or BAFF plus BR3-Fc (BAFF antagonist). The apoptosis of CD4 cells and CD8 cells was analyzed by flow cytometry. CD4 cells and CD8 cells were isolated from peripheral blood of COPD patients respectively and treated with BAFF or BAFF plus BR3-Fc. Interferon-γ (IFN-γ) and interleukin-4 (IL-4) were detected in the CD4 cells, and perforin and granzyme B were detected in the CD8 cells.
BAFF expression was increased in the cells of sputum and the plasma from COPD patients compared with control subjects. The plasma BAFF levels were inversely correlated with FEV percentage of predicted in patients with COPD. BAFF did not significantly alter the apoptosis of CD4 cells, however it significantly inhibited the apoptosis of CD8 cells from COPD patients. BAFF increased IFN-γ expression in the CD4 cells from COPD patients, while it did not significantly alter the expresson of IL-4 in these cells. BAFF increased the expression of perforin and granzyme B in the CD8 cells from COPD patients.
Our findings indicate that BAFF may be involved in the inflammatory response in COPD via affecting T lymphocytes, suggesting a possible role of BAFF in the pathogenesis of COPD.
据报道,B 细胞激活因子属于肿瘤坏死因子家族(BAFF)在慢性阻塞性肺疾病(COPD)中的表达增加。然而,其在这种慢性炎症性疾病中的作用尚不完全清楚。先前的研究表明,BAFF 也会影响 T 细胞功能。因此,我们研究了 BAFF 对 COPD 患者 T 淋巴细胞的影响。
检测痰和血浆中的 BAFF。从 COPD 患者中分离外周血单个核细胞(PBMCs),并用 BAFF 或 BAFF 加 BR3-Fc(BAFF 拮抗剂)处理。通过流式细胞术分析 CD4 细胞和 CD8 细胞的凋亡。分别从 COPD 患者的外周血中分离 CD4 细胞和 CD8 细胞,并用 BAFF 或 BAFF 加 BR3-Fc 处理。检测 CD4 细胞中的干扰素-γ(IFN-γ)和白细胞介素-4(IL-4),检测 CD8 细胞中的穿孔素和颗粒酶 B。
与对照组相比,COPD 患者痰和血浆中的 BAFF 表达增加。COPD 患者的血浆 BAFF 水平与 FEV 预测百分比呈负相关。BAFF 对 CD4 细胞的凋亡无显著影响,但明显抑制 COPD 患者 CD8 细胞的凋亡。BAFF 增加 COPD 患者 CD4 细胞中 IFN-γ的表达,而对这些细胞中 IL-4 的表达无显著影响。BAFF 增加 COPD 患者 CD8 细胞中穿孔素和颗粒酶 B 的表达。
我们的研究结果表明,BAFF 可能通过影响 T 淋巴细胞参与 COPD 的炎症反应,提示 BAFF 可能在 COPD 的发病机制中起作用。