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慢性阻塞性肺疾病中气道和肺实质的炎症:T细胞的作用。

Inflammation of the airways and lung parenchyma in COPD: role of T cells.

作者信息

Cosio Manuel G, Majo Joaquim, Cosio Monica G

机构信息

Respiratory Division, McGill University, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, PQ H3A 1A1, Canada.

出版信息

Chest. 2002 May;121(5 Suppl):160S-165S. doi: 10.1378/chest.121.5_suppl.160s.

DOI:10.1378/chest.121.5_suppl.160s
PMID:12010846
Abstract

A smoking-induced inflammatory reaction in the airways and lung parenchyma, comprised mainly of neutrophils and alveolar macrophages, has long been accepted to be the major cause of COPD in smokers. Recent reports have underlined the role of the T lymphocyte as a potentially important factor in the inflammatory process leading to COPD. It has been found that, in the airways and the lung parenchyma, the presence of T cells, predominantly CD8+ T cells, can distinguish between smokers with and without COPD. In addition to T cells, other inflammatory cell types such as neutrophils and macrophages are probably essential in the initial inflammatory process leading to the breakdown of lung tissue, perhaps producing peptides eventually recognized by T cells as antigenic. This would provide an explanation for the T-cell inflammation. Once activated, T cells are present in the lung, and their effector functions would include the attraction and enhancement of the inflammatory function in other inflammatory cells like neutrophils and macrophages. It seems likely that, only when all inflammatory cell types (ie, CD4+, CD8+, neutrophils, and macrophages) are present in the lung, the airways remodeling and parenchymal destruction characteristic of COPD will ensue. If T cells are responsible for the lung injury and progression of COPD, it would resemble a response to an antigenic stimulus originating in the lung. If that were the case, COPD could be considered to be an autoimmune disease triggered by smoking.

摘要

长期以来,人们一直认为,气道和肺实质中由中性粒细胞和肺泡巨噬细胞主导的吸烟引发的炎症反应是吸烟者患慢性阻塞性肺疾病(COPD)的主要原因。最近的报告强调了T淋巴细胞在导致COPD的炎症过程中作为潜在重要因素的作用。研究发现,在气道和肺实质中,T细胞(主要是CD8 + T细胞)的存在可以区分患有和未患有COPD的吸烟者。除了T细胞外,其他炎症细胞类型,如中性粒细胞和巨噬细胞,可能在导致肺组织破坏的初始炎症过程中至关重要,也许会产生最终被T细胞识别为抗原的肽。这将为T细胞炎症提供一种解释。一旦被激活,T细胞就会出现在肺部,其效应功能将包括吸引和增强其他炎症细胞(如中性粒细胞和巨噬细胞)的炎症功能。似乎只有当肺部存在所有炎症细胞类型(即CD4 +、CD8 +、中性粒细胞和巨噬细胞)时,才会出现COPD特有的气道重塑和实质破坏。如果T细胞导致肺损伤和COPD进展,这将类似于对源自肺部的抗原刺激的反应。如果是这样,COPD可以被认为是一种由吸烟引发的自身免疫性疾病。

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