Abnormal peripheral blood T-lymphocyte subsets in a subgroup of patients with COPD.

BACKGROUND: Smoking may induce changes in T-lymphocyte subsets in peripheral blood. Abnormalities of T-lymphocyte subsets in peripheral blood and in BAL fluid, and increased CD8+ T lymphocytes in the airways have been reported in patients with COPD. These findings suggest that T-lymphocyte abnormalities might be involved in the pathogenesis of airflow limitation in people who smoke.
DESIGN: Cross-sectional study.
SETTING: Outpatient pulmonary department of a university hospital.
METHODS: To investigate this hypothesis, peripheral blood T-lymphocyte subsets were measured by flow cytometry using specific monoclonal antibodies in 20 healthy nonsmokers, 20 healthy smokers, and 20 smokers with stable COPD. No significant differences in the peripheral blood T-lymphocyte subsets were observed among the three groups. Because a previous study showed peripheral blood T-lymphocyte abnormalities in the subgroup of nonsmoking patients with COPD, we wanted to investigate what factors determine the subgroup of COPD with abnormal T-lymphocyte subsets. We tried to measure the relationship between T-lymphocyte subsets and physiologic indexes of pulmonary function tests in patients with COPD. The proportion of CD8+ T lymphocytes significantly correlated with diffusing capacity of the lung for carbon monoxide (DLCO) and DLCO per unit of alveolar volume (DLCO/VA), and CD4+/CD8+ ratio correlated with DLCO/VA. Therefore, we attempted to classify the patients with COPD into two subgroups on the basis of DLCO/VA: 10 COPD patients with low DLCO/VA (< 80% predicted) and 10 patients with normal DLCO/VA (> or = 80% predicted).
RESULTS: The normal DLCO/VA subgroup had a significantly higher proportion of CD8+ T lymphocytes and a lower CD4+/CD8+ ratio than the healthy smokers or the low DLCO/VA subgroup. Moreover, FEV1/FVC significantly correlated with the CD4+/CD8+ ratio only in the normal DLCO/VA subgroup.
CONCLUSION: These findings suggest that T-lymphocyte abnormalities might be involved in the pathogenesis of airflow limitation in a subgroup of patients with COPD, presumably with small airways disease, but not in all cases of COPD.