γδ T-cells and the peripheral blood T-cell profile in pulmonary tuberculosis, chronic obstructive pulmonary disease, and their comorbidity
TL;DR
Isolated TB was associated with elevated CD3 + /αβ-T-cell counts, whereas COPD and TB + COPD were associated with their reduction and a selective deficit of γδ-T-cells.
Abstract
Introduction. The combination of chronic obstructive pulmonary disease (COPD) and pulmonary tuberculosis (TB) is a clinically significant comorbidity. The role of αβ- and γδ-T-cell immunity in their isolated and combined course remains insufficiently studied. Aim. To establish features of the subpopulation composition of peripheral blood Tlymphocytes in isolated COPD, isolated TB, their combination, and in conditionally healthy individuals, as well as to identify associations between the T-cell profile and indicators of pulmonary ventilation function and systemic inflammation. Materials and methods. Using flow cytometry in 55 men (TB – 17, COPD – 16, TB + COPD – 8, control group – 14), the relative proportions of CD3 + -, αβ- (CD3 + TCRγδ - ), and γδ- (CD3 + TCRγδ + ) T-lymphocytes were determined; absolute counts (×10 9 /L) were calculated using a two-platform method based on complete blood count data. The Kruskal–Wallis test with Dunn's post-hoc test and Holm correction, Cliff's δ effect size, Spearman correlations with Benjamini–Hochberg correction, and sensitivity analysis with exclusion of two observations with extremely low relative CD3 + content in the TB + COPD group were used. Results. The relative counts of CD3 + T-lymphocytes differed significantly between groups (H = 24.1; p < 0.001): maximum in isolated TB (19.4%), minimum in TB + COPD (11.8%; Cliff's δ = 1.00 when compared with TB). The absolute counts of CD3 + T-lymphocytes confirmed these differences: 1.71 × 10 9 /L in TB versus 1.00 in TB + COPD and 0.95 in COPD (p = 0.002). The proportion of γδ T-lymphocytes within the CD3 + pool decreased in patients with bronchopulmonary pathology (2.1–3.2%) compared to controls (6.9%); significance was maintained for TB (p < 0.01) and COPD (p < 0.001). CD3 + T-cells positively correlated with the forced expiratory volume in 1 second to forced vital capacity ratio (FEV 1 /FVC) (ρ = 0.60) and FEV 1 (ρ = 0.48), and negatively with smoking history (ρ = −0.54), neutrophil-to-lymphocyte ratio (NLR), and IL-1β (both ρ = −0.47); all differences persisted in the sensitivity analysis. Conclusion. Isolated TB was associated with elevated CD3 + /αβ-T-cell counts, whereas COPD and TB + COPD were associated with their reduction and a selective deficit of γδ-T-cells. Shifts in the T-cell profile are linked to the severity of bronchial obstruction, smoking history, and systemic inflammation. This allows consideration of the T-cell profile as a potential immunological marker of the broncho-obstructive phenotype in TB; however, confirmation of causal relationships requires prospective studies.