调节性T细胞在慢性阻塞性肺疾病中的作用

IF 2 Q3 RESPIRATORY SYSTEM
Pulmonary Medicine Pub Date : 2025-03-06 eCollection Date: 2025-01-01 DOI:10.1155/pm/5048054
Meghashree Sampath, Geetanjali Bade, Randeep Guleria, Anant Mohan, Sudip Sen, Anjana Talwar
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引用次数: 0

摘要

背景:慢性阻塞性肺疾病(COPD)是一种以可逆性较差的气道阻塞为特征的进行性肺部疾病。慢性阻塞性肺病是一种炎症性疾病,其促炎因子和抗炎因子之间存在不平衡。调节性T细胞(Regulatory T cells, Tregs)作为免疫反应的负调节因子,在其他炎症性疾病和炎症动物模型中也发挥着重要作用。目的:本研究旨在评估循环Tregs的抑制功能,并检测初始CD4+ T细胞诱导产生诱导Tregs的能力。方法:研究对象为20例COPD患者(吸烟者10例;戒烟者n = 10)和20名年龄匹配的健康对照者(吸烟者n = 10;非吸烟者n = 10)。采用Ficoll密度梯度分离法分离外周血单个核细胞。通过评估T反应细胞(CD4+CD25-)在循环Tregs (CD4+CD25+)存在下在多克隆刺激下的增殖来评估其抑制功能。此外,在抑制实验的培养上清中评估细胞因子介导的抑制。通过刺激初始CD4+ T细胞在抗cd3、IL-2和TGF-β1存在下产生iTregs来评估诱导能力。结果:与对照组相比,COPD吸烟者(p = 0.03)和COPD改造吸烟者(p = 0.04)中Tregs对T反应细胞的抑制百分比显著降低。在细胞因子介导的抑制评估中,抑制实验培养上清中观察到COPD S中IL-2较COPD RS显著降低(p < 0.05), COPD S中IL-10和TGFß1较CNS显著降低(p < 0.05), CS显著降低(p < 0.05)。此外,与COPD RS相比,COPD S中CD4+CD25+CD45RA+CD127-表型的iTregs频率显著更高(p < 0.01)。讨论:观察COPD患者的特征变化。尽管全身炎症增加,但Tregs功能受损表明这些细胞在疾病发病机制中的潜在作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of Regulatory T Cells in Chronic Obstructive Pulmonary Disease.

Background: Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder characterized by poorly reversible airway obstruction. COPD being an inflammatory disorder has been proposed to have an imbalance between proinflammatory and anti-inflammatory factors. Regulatory T cells (Tregs) being a negative regulator of immune response have been observed to play an important role in other inflammatory diseases as well as animal models of inflammation. Objective: This study is aimed at assessing the suppressive functions of circulatory Tregs and examining the inductive capacity of naive CD4+ T cells to generate induced Tregs. Methods: The study was conducted in 20 COPD patients (smokers n = 10; reformed smokers n = 10) and 20 age-matched healthy controls (smokers n = 10; nonsmokers n = 10). Peripheral blood mononuclear cells were isolated from blood using Ficoll density gradient separation. The suppressive functions were evaluated by assessing the proliferation of T responder cells (CD4+CD25-) in the presence of circulatory Tregs (CD4+CD25+) under polyclonal stimulation. In addition, cytokine-mediated suppression was assessed in the culture supernatants of the suppression assay. Inductive capacity was assessed by stimulating naive CD4+ T cells to generate iTregs in the presence of anti-CD3, IL-2, and TGF-β1. Results: The percent suppression of T responder cells by Tregs was significantly lower in COPD smokers (p = 0.03) and COPD reformed smokers (p = 0.04) as compared to control smokers. On the assessment of cytokine-mediated suppression, significantly reduced IL-2 in COPD S as compared to COPD RS (p < 0.05) and reduced IL-10 and TGFß1 in COPD S as compared to CNS (p < 0.05) and CS (p < 0.05) was observed in the culture supernatants of suppression assay. In addition, a significantly higher frequency of iTregs with phenotype CD4+CD25+CD45RA+CD127- was observed in COPD S as compared to COPD RS (p < 0.01). Discussion: Characteristics changes were observed in patients with COPD. The compromised Tregs function, despite the increase in systemic inflammation, suggests a potential role of these cells in the pathogenesis of the disease.

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来源期刊
Pulmonary Medicine
Pulmonary Medicine RESPIRATORY SYSTEM-
CiteScore
10.20
自引率
0.00%
发文量
4
审稿时长
14 weeks
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