CD4(+)CD25(-)Foxp3(+) T cells play a role in tuberculous hydrothorax rather than malignant hydrothorax.

BACKGROUND: Foxp3(+) T cells regulate inflammation and tumorigenesis. However, little is known about the role of different subsets of Foxp3(+) T cells in malignant or tuberculous hydrothorax. METHODS: The numbers of CD4(+)CD25(+)Foxp3(+), CD4(+)CD25(-)Foxp3(+) T cells and the levels of some inflammatory cytokines in patients with tuberculous hydrothorax, malignant hydrothorax, and healthy controls (HCs) were examined by flow cytometry and ELISA. The potential association between the numbers of different subsets of Foxp3 + T cells and the values of clinical measures were analyzed. RESULTS: The numbers of peripheral blood CD4(+)CD25(+)Foxp3(+) T cells were greater in malignant hydrothorax patients than in HCs, but fewer than those of hydrothorax in patients. The percentages of circulating IL-10(+) or LAP(+) CD4(+)CD25(+)Foxp3(+) T cells were higher than in the hydrothorax in patients with malignant hydrothorax. The numbers of circulating CD4(+)CD25(-)Foxp3(+) T cells were significantly fewer in patients with tuberculous hydrothorax than in HCs, and both the numbers of circulating CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were significantly fewer than in the hydrothorax in patients. Significantly higher percentages of circulating IL-10(+) or LAP(+) CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were detected in tuberculous hydrothorax patients. The numbers of CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were associated with hydrothorax adenosine deaminase (ADA) levels in tuberculous hydrothorax patients, while CD4(+)CD25(+)Foxp3(+) T cells were associated with carcino-embryonic antigen (CEA) in malignant hydrothorax patients. The concentrations of serum IL-6 and TGF-ß in the patients were significantly higher than that in the HCs, but lower than that in the corresponding hydrothorax. A similar pattern of IL-10 was observed in different groups, except that there was no significant difference in the levels of serum IL-10 between the tuberculous hydrothorax patients and HCs. CONCLUSIONS: CD4(+)CD25(-)Foxp3(+) T cells, which have lower inhibitory function than CD4(+)CD25(+)Foxp3(+) T cells, may play a role in tuberculous hydrothorax.

Different subsets of macrophages in patients with new onset tuberculous pleural effusion.

OBJECTIVE: Macrophages are the infiltrate components of tuberculous pleural effusion (TPE). This study is aimed at examining the role of different subsets of macrophages in pleural fluid (PF) and peripheral blood (PB) from patients with new onset TPE. METHODS: The numbers of PB and PF CD163(+), CD206(+) and CD115(+) macrophages in 25 patients with new onset TPE and 17 healthy controls (HC) were determined by flow cytometry. The concentrations of serum and PF cytokines were determined by cytometric bead array (CBA) and enzyme-linked immunosorbentassay (ELISA). The potential association between the numbers of different subsets of macrophages and the values of clinical measures in TPE patients were analyzed. RESULTS: The numbers of PB CD14(+)CD163(-) M1-like and CD14(+)CD163(-) interleukin (IL)-12(+) M1 macrophages were significantly higher than that in the HC, but lower than PF, and the numbers of PF CD14(+)CD163(+), CD14(+)CD163(+)CD206(+), CD14(+)CD163(+)CDll5(+) M2-like, and CD14(+)CD163(+)IL-10(+) M2 macrophages were less than PB in the TPE patients. The levels of serum IL-1, IL-6, IL-8, IL-12, tumor growth factor (TGF)-ß1, and tumor necrosis factor (TNF)-α in the TPE patients were significantly higher than that in the HC, but lower than that in the PF. The levels of PF IL-10 were significantly higher than that in the PB of patients and HC. In addition, the levels of serum IL-12 and TNF-α were correlated positively with the values of erythrocyte sedimentation rate (ESR) and the numbers of ESAT-6- and culture filtrate protein 10 (CFP-10)-specific IFN-γ-secreting T cells, and the levels of PF TNF-α were correlated positively with the levels of PF adenosine deaminase (ADA) and lactate dehydrogenase (LDH) in those patients. CONCLUSION: Our data indicate that Mycobacterium tuberculosis (M. tb) infection induces M1 predominant pro-inflammatory responses, contributing to the development of TPE in humans.