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Inflammation of the Airways and Lung Parenchyma in COPD*: Role of T Cells

Manuel G. Cosio, MD; Joaquim Majo, MD; Monica G. Cosio, MD
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*From the McGill University (Dr. Manuel Cosio), Royal Victoria Hospital, Montreal, PQ, Canada; the Department d’Anatomia Patologica (Dr. Majo), Hospitals Universitaris Vall d’Hebron, Barcelona, Spain; and the Department of Pathology (Dr. Monica Cosio), Ramon y Cajal University Hospital, Madrid, Spain.

Correspondence to: Manuel G. Cosio, MD, Professor of Medicine, McGill University, Royal Victoria Hospital, Respiratory Division, Room L4.11, 687 Pine Ave West, Montreal, PQ H3A 1A1 Canada; e-mail: manuel.cosio@muhc.mcgill.ca



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

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