Abstract
BackgroundFoxp3+ 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.MethodsThe 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.ResultsThe 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-β 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.ConclusionsCD4+CD25−Foxp3+ T cells, which have lower inhibitory function than CD4+CD25+Foxp3+ T cells, may play a role in tuberculous hydrothorax.
Highlights
the forkhead family transcription factor (Foxp3)+ T cells regulate inflammation and tumorigenesis
The numbers of peripheral blood CD4+CD25+Foxp3+ T cells were greater in malignant hydrothorax patients than in healthy controls (HCs), but fewer than those of hydrothorax in patients
The num‐ bers 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 sig‐ nificantly fewer than in the hydrothorax in patients
Summary
Foxp3+ T cells regulate inflammation and tumorigenesis. Little is known about the role of dif‐ ferent subsets of Foxp3+ T cells in malignant or tuberculous hydrothorax. Tang et al J Transl Med (2015) 13:268 in the pathogenesis of malignant hydrothorax and tuberculous hydrothorax. Treg are characterized by CD4+CD25+ [6] and express the forkhead family transcription factor (Foxp3), which is necessary for the development and function of Tregs [7–9]. Foxp has been described as a highly specific intracellular marker for Tregs. The CD4+CD25+FoxP3+ Tregs have potent suppressive activity to prevent pathogenic damage under inflammatory conditions, and they have the tendency to keep tumors from host immunologic surveillance [10–12]. CD4+CD25+FoxP3+ Tregs can promote immune escape of tumor cells and Mycobacterium tuberculosis (M.tb). High percentages of CD4+CD25+FoxP3+ Tregs have been found in the hydrothorax of patients with tuberculous hydrothorax and malignant hydrothorax [13, 14].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
