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Increase of Th17 cells in peripheral blood of patients with chronic obstructive pulmonary disease
María Inés Vargas-Rojas1, Alejandra Ramírez-Venegas, Leonardo Limón-Camacho
1COPD and Smoking Cessation Clinics, Instituto Nacional de Enfermedades Respiratorias, Ismael Cosío Villegas, INER, Tlalpan 4502, Mexico 14080, Mexico. manecbba@yahoo.com
Background:
Chronic obstructive pulmonary disease (COPD) is a progressive disorder characterized by an inflammatory response to cigarette smoke. A disorder in immune regulation contributing to the pathogenesis of COPD has been suggested, however, little is known about the involvement of CD4 (+) T cells. To determine the distribution of different CD4(+) T cell subsets in patients with COPD, current smokers without COPD (CS) and healthy subjects (HS), and its correlation with pulmonary function.
Methods:
Th1, Th2, Th17 and Treg, subsets, were quantified by flow cytometry in peripheral blood (PB) of 39 patients with COPD, 14 CS and 15 HS. Correlations were assessed with Spearman's rank test. The association between Th17 and lung function was evaluated with a multivariate logistic regression analysis.
Results:
An increase of Th17 cells (median 9.7% range 0.8-22.5%) was observed in patients with COPD compared with CS (median 2.8% range 0.8-10.6) and HS (median 0.6% range 0.4-1%, p < 0.0001). Th1 and Tregs subsets were also increased in COPD and CS compared to HS. Inverse correlations were found between Th17 with FEV(1)%p r = -0.57 and with FEV(1)/FVC r = -0.60, (p < 0.0001 for both comparison). In addition, increase of Th17 predicted the presence [OR 1.76 (CI 95% 1.25-2.49, p = 0.001)] and severity of airflow limitation [OR 1.13 (CI95% 1.02-1.25, p = 0.02)].
Conclusions:
The increase of Th17 response and the lost of balance between CD4(+) T cell subsets, suggest a lack of regulation of the systemic inflammatory response that may contribute to pathogenesis in COPD patients.
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