Cytotoxic CD8+ T cells have been suggested to be key players in the pathogenesis of chronic obstructive pulmonary disease (COPD). We wanted to investigate the phenotype of lung tissue T lymphocytes (LTL) and tumour-infiltrating T lymphocytes (TIL) in smokers with peripheral non-small cell lung carcinoma (NSCLC) with moderate/severe versus mild COPD. Lung tissue and tumour samples were obtained from patients with moderate/severe stage of COPD (n = 10) and from patients with mild stage of COPD (n = 7) at lung resection for a solitary peripheral NSCLC, processed and analysed by flow cytometry. The flow-cytometric results showed that lung tissue T cells, regardless of the severity of COPD, were mostly of the activated phenotype, expressed the CXCR3 chemokine receptor characteristic of type 1 T cells, and did neither significantly differ in the expression of activation markers (CD69, CD25 and HLA-DR), differentiation markers (CD27 and CD28) and chemokine receptors (CXCR3 and CCR4) between the selected groups, nor showed any significant correlation with lung function measured as forced expiratory volume in 1 s (FEV1) or TLCO. Compared with LTL, a significantly greater proportion of TIL expressed the activation markers CD69 and CD25, but a lower proportion showed a fully differentiated CD27-28- phenotype. We conclude that lung LTL patterns are similar in NSCLC patients with moderate/severe or mild stages of COPD, and are not significantly related to lung function. LTL and TIL possess different phenotype characteristics. The majority of tumour tissue T cells are activated, but it seems that their process of differentiation is incomplete. © 2007 The Authors.
CITATION STYLE
Marc, M. M., Korosec, P., Kern, I., Sok, M., Ihan, A., & Kosnik, M. (2007). Lung tissue and tumour-infiltrating T lymphocytes in patients with non-small cell lung carcinoma and chronic obstructive pulmonary disease (COPD): Moderate/severe versus mild stage of COPD. Scandinavian Journal of Immunology, 66(6), 694–702. https://doi.org/10.1111/j.1365-3083.2007.02018.x
Mendeley helps you to discover research relevant for your work.