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Eur Respir J 2005; 25:441-446
Copyright ©ERS Journals Ltd 2005

Blunted {gamma}{delta} T-lymphocyte response in chronic obstructive pulmonary disease

J. Pons1,2, J. Sauleda3, J. M. Ferrer2, B. Barceló4, A. Fuster2, V. Regueiro1, M. R. Julià2 and A. G. N. Agustí1,3

1 Unidad de Investigación, 2 Inmunología, 3 Neumología, and 4 Análisis Clinicos, Hospital Universitario Son Dureta, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Palma de Mallorca, Spain

CORRESPONDENCE: A. G. N. Agustí, Servei de Pneumologia, Hospital Universitari Son Dureta, Andrea Doria 55, 07014- Palma de Mallorca, Spain. Fax: 34 971175228. E-mail: aagusti@hsd.es

Keywords: Flow cytometry, lung inflammation, mucosal homeostasis, tissue repair

Received: June 10, 2004
Accepted November 28, 2004

Chronic obstructive pulmonary disease (COPD) is characterised by an excessive inflammatory response to inhaled particles, mostly tobacco smoking. Although inflammation is present in all smokers, only a percentage of them develop COPD. T-lymphocytes are important effector and regulatory cells that participate actively in the inflammatory response of COPD. They comprise the T-cell receptor (TCR)-{alpha}ß (CD4+ and CD8+) and TCR-{gamma}{delta} T-lymphocytes. The latter represent a small percentage of the total T-cell population, but play a key role in tissue repair and mucosal homeostasis.

To investigate TCR-{alpha}ß (CD4+ and CD8+) and TCR-{gamma}{delta} T-lymphocytes in COPD, the present authors determined, by flow cytometry, the distribution of both subpopulations in peripheral blood and bronchoalveolar lavage (BAL) samples obtained from patients with COPD, smokers with normal lung function and never-smokers.

The present study found that: 1) the distribution of CD4+ and CD8+ lymphocytes in blood and BAL was similar in all three groups; 2) compared with nonsmokers, {gamma}{delta} T-lymphocytes were significantly increased in smokers with preserved lung function; and 3) this response was blunted in patients with COPD.

These results highlight a novel, potentially relevant, pathogenic mechanism in chronic obstructive pulmonary disease.




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