Decrease in CD4+CD25+FoxP3+ Treg cells after pulmonary resection in the treatment of cavity multidrug-resistant tuberculosis

Wu, Ying; Wen, Peng; Cai, Ying; Zheng, Gao Zhe; Zheng, Geng Long; Lin, Jing; Zhang, Su Wei; Li, Ké

doi:10.1016/j.ijid.2010.04.005

Cited by 24 publications

(14 citation statements)

References 17 publications

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“…It has been previously reported that patients with TB have a high proportion of circulating T reg cells of the CD4 + CD25 + FOXP3 + phenotype compared with patients with LTBI or uninfected controls (7,8). A previous study by our group revealed that the elevated numbers of CD4 + CD25 + FOXP3 + cells observed in MDR-TB were found to decrease following removal of the M. tuberculosis burden by pulmonary resection (9), which demonstrated that the increase in FOXP3 + T reg cells is a potential mechanism by which M. tuberculosis evades immune eradication. In individuals with tuberculosis, these cells have been observed to suppress the T-cell response to mycobacterial antigens, whereas the CD4 + CD25 + FOXP3 + cells from non-healthy individuals do not suppress the secretion of IFN-γ induced by protective mycobacterial antigens (8,23).…”

Section: Discussionmentioning

confidence: 73%

“…Several previous studies have found that the number of FOXP3 + T reg cells is increased in patients with active TB and are expanded at sites of active disease, where containment of inflammation and immune-mediated pathology is required most (7,8). A previous study by our group demonstrated that elevated levels of FOXP3 + T reg cells decreased following pulmonary resection in patients with pulmonary multiplicitous drug resistant tuberculosis (MDR-TB) (9). This suggested that FOXP3 + cells may be essential during TB development; however, the mechanism underlying the increased levels of FOXP3 + cells in active TB patients remains to be elucidated.…”

Section: Introductionmentioning

confidence: 98%

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Effective expansion of forkhead box P3+ regulatory T cells via early secreted antigenic target 6 and antigen 85 complex B from Mycobacterium tuberculosis

Cai

et al. 2014

Molecular Medicine Reports

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The expansion of CD4+ CD25+ forkhead box (FOX)P3+ regulatory T (Treg) cells has been observed in patients with Mycobacterium (M.) tuberculosis; however, the mechanism of expansion remains to be elucidated. The aim of the present study was to examine the role of the early secreted antigenic target 6(ESAT‑6) and antigen 85 complex B (Ag85B) from M. tuberculosis on Treg cell expansion. To investigate the sensitivity of peripheral blood cultures to the M. tuberculosis ESAT‑6 and Ag85B antigens, the proportion of circulating CD4+ CD25+ FOXP3+ Treg cells was determined using flow cytometry and the levels of FOXP3 mRNA were determined using reverse transcription quantitative polymerase chain reaction. The mRNA levels of FOXP3 and the proportion of circulating CD4+ CD25+ FOXP3+ Treg cells were increased in multiplicitous drug‑resistant tuberculosis patients compared with those in healthy controls and patients with latent tuberculosis (TB) infection (LTBI) (P<0.001). The mycobacterial antigens ESAT‑6 and Ag85B increased the expansion of the CD4+ CD25+ FOXP3+ Treg cells and the mRNA levels of FOXP3 in healthy controls and LTBI patients compared with the effect of Bacillus Calmette‑Guerin (P<0.05). Additionally, the mRNA levels of FOXP3 were elevated in the LTBI patients following stimulations with the mycobacterial antigens (P=0.012). Therefore, the M. tuberculosis antigens ESAT‑6 and Ag85B induced CD4+ CD25+ FOXP3+ Treg‑cell expansion, particularly in patients with LTBI. These findings indicated that CD4+ CD25+ FOXP3+ Treg cells may have a primary role in the failure of the host immune system to eradicate M. tuberculosis.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 98%

Effective expansion of forkhead box P3+ regulatory T cells via early secreted antigenic target 6 and antigen 85 complex B from Mycobacterium tuberculosis

Cai

et al. 2014

Molecular Medicine Reports

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“…In active TB, the immunological balance fails, inflammation increases and larger numbers of Treg cells are recruited to the site of infection, indicated by higher frequencies of circulating Treg cells [18,19,28,29,36]. Supporting this finding, infected macaques show decreasing numbers of circulating Treg cells during the first weeks following infection, as these are recruited to the lung.…”

Section: Discussionmentioning

confidence: 76%

“…In TB, the numbers of circulating Treg cells decrease after resection of pulmonary cavities [36]. Therefore, Treg cells or their surrogate markers (TGF-b1 and IL-10) merit further investigation for the monitoring of TB treatment response.…”

Section: Discussionmentioning

confidence: 99%

Increased frequencies of pulmonary regulatory T-cells in latentMycobacterium tuberculosisinfection

Herzmann

Ernst²,

Ehlers

et al. 2012

Eur Respir J

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Regulation of specific immune responses following exposure to Mycobacterium tuberculosis in humans and the role of regulatory T (Treg) cells in the immune control of latent infection with M. tuberculosis are incompletely understood.Latent infection was assayed by an interferon-c release assay (IGRA) in healthcare workers regularly exposed to tuberculosis (TB) patients and in household TB contacts in Germany. Immunophenotypes of bronchoalveolar lavage (BAL) mononuclear cells and peripheral blood mononuclear cells (PBMCs) were analysed by fluorescence-activated cell sorting.All TB contacts with latent infection (n515) had increased (p,0.0001) frequencies of CD4+ CD25+ CD127-Treg cells (median 2.12%, interquartile range (IQR) 1.63-3.01%) among BAL mononuclear cells compared with contacts (n525) with negative IGRA results (median 0.68%, IQR 0.32-0.96%) No differences were seen when PBMC immunophenotypes of IGRA+ and IGRA-TB contacts were compared (IGRA+ median 9.6%, IQR 5.9-10.1%; IGRA-median 7.7%, IQR 4.6-11.3%; p50.47). Five out of 25 contacts with negative blood IGRAs showed a positive IGRA from BAL cells, possibly indicating a limited local immune response.In Germany, latent infection with M. tuberculosis, as defined by a positive M. tuberculosisspecific IGRA response on cells from the peripheral blood, is characterised by an increased frequency of Treg cells in the BAL.

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“…peripheral T-regulatory cells, exhaustion T cells) and inflammatory proteins (i.e. vascular endothelial growth factor, interferon-γ-inducible protein 10) in the course of treatment was also described [96,97,98]. Biomarkers or compound markers consisting of blood markers, radiological assessment by chest X-ray, CT or positron emission tomography-CT, and clinical scores could eventually help to subsequently individualize the duration of therapy for patients affected by chronic respiratory infections [14,99,100].…”

Section: Future Perspective: Personalized Medicine To Improve Clinicamentioning

confidence: 99%

Personalized Medicine for Chronic Respiratory Infectious Diseases: Tuberculosis, Nontuberculous Mycobacterial Pulmonary Diseases, and Chronic Pulmonary Aspergillosis

et al. 2016

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Chronic respiratory infectious diseases are causing high rates of morbidity and mortality worldwide. Tuberculosis, a major cause of chronic pulmonary infection, is currently responsible for approximately 1.5 million deaths per year. Although important advances in the fight against tuberculosis have been made, the progress towards eradication of this disease is being challenged by the dramatic increase in multidrug-resistant bacilli. Nontuberculous mycobacteria causing pulmonary disease and chronic pulmonary aspergillosis are emerging infectious diseases. In contrast to other infectious diseases, chronic respiratory infections share the trait of having highly variable treatment outcomes despite longstanding antimicrobial therapy. Recent scientific progress indicates that medicine is presently at a transition stage from programmatic to personalized management. We explain current state-of-the-art management concepts of chronic pulmonary infectious diseases as well as the underlying methods for therapeutic decisions and their implications for personalized medicine. Furthermore, we describe promising biomarkers and techniques with the potential to serve future individual treatment concepts in this field of difficult-to-treat patients. These include candidate markers to improve individual risk assessment for disease development, the design of tailor-made drug therapy regimens, and individualized biomarker-guided therapy duration to achieve relapse-free cure. In addition, the use of therapeutic drug monitoring to reach optimal drug dosing with the smallest rate of adverse events as well as candidate agents for future host-directed therapies are described. Taken together, personalized medicine will provide opportunities to substantially improve the management and treatment outcome of difficult-to-treat patients with chronic respiratory infections.

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Decrease in CD4+CD25+FoxP3+ Treg cells after pulmonary resection in the treatment of cavity multidrug-resistant tuberculosis

Abstract: Circulating T(reg) cells are increased in proportion in patients with cavity MDR-TB and decreased after surgery. Infection with M. tuberculosis may induce T(reg) cell-surface molecular changes with increased numbers of cells.

Cited by 24 publications

References 17 publications

Effective expansion of forkhead box P3+ regulatory T cells via early secreted antigenic target 6 and antigen 85 complex B from Mycobacterium tuberculosis

Effective expansion of forkhead box P3+ regulatory T cells via early secreted antigenic target 6 and antigen 85 complex B from Mycobacterium tuberculosis

Increased frequencies of pulmonary regulatory T-cells in latentMycobacterium tuberculosisinfection

Personalized Medicine for Chronic Respiratory Infectious Diseases: Tuberculosis, Nontuberculous Mycobacterial Pulmonary Diseases, and Chronic Pulmonary Aspergillosis

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