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Article

FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients

  • Authors:
    • Jian‑Guo Zhang
    • Xiao‑Juan Chen
    • Tao Liu
    • Shu‑Juan Jiang
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory Medicine, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, P.R. China, Department of Neurology, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China, Department of Critical Care Medicine, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China
  • Pages: 2753-2758
    |
    Published online on: September 6, 2016
       https://doi.org/10.3892/etm.2016.3662
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Abstract

Asthma is a chronic bronchial inflammation that results to reversible incidence of airway obstruction and shortness of breath. Under normal circumstances, the lung immune system is maintained in a state of controlled inflammation, where balance exists between protective immunity mediated by effector cells and tolerance mediated by cells with regulatory function. Therefore, the inflammation observed in asthma patients may be caused by an imbalance between regulatory T (Treg) cells (CD4‑positive with high expression of CD25 surface markers) and forkhead box P3 (FOXP3)-positive pro-inflammatory T helper 17 (Th17) cells. The aim of the present study was to evaluate whether reduced Treg cells and increased Th17 cells could be observed in the peripheral blood samples of asthma patients. As important markers of Treg cells, the expression levels of FOXP3 and interleukin (IL)‑17a were analyzed via reverse trancription-quantitative polymerase chain reaction. The results indicated that the levels of cytokines that promote Th17 cells, including IL‑6, IL‑23 and TGF‑β, were found to increase in the bronchoalveolar lavage fluid sample of asthma patients. However, the IL‑10 level in the corresponding sample was much lower compared with that in control individuals. In conclusion, these results suggest that asthma associated with a reduced proportion of Treg and Th17 cells in the blood is characterized by the expression of pro‑inflammatory cytokines that may be beneficial for the continuous generation of Th17 cells.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang JG, Chen XJ, Liu T and Jiang SJ: FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients. Exp Ther Med 12: 2753-2758, 2016.
APA
Zhang, J., Chen, X., Liu, T., & Jiang, S. (2016). FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients. Experimental and Therapeutic Medicine, 12, 2753-2758. https://doi.org/10.3892/etm.2016.3662
MLA
Zhang, J., Chen, X., Liu, T., Jiang, S."FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients". Experimental and Therapeutic Medicine 12.4 (2016): 2753-2758.
Chicago
Zhang, J., Chen, X., Liu, T., Jiang, S."FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients". Experimental and Therapeutic Medicine 12, no. 4 (2016): 2753-2758. https://doi.org/10.3892/etm.2016.3662
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang JG, Chen XJ, Liu T and Jiang SJ: FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients. Exp Ther Med 12: 2753-2758, 2016.
APA
Zhang, J., Chen, X., Liu, T., & Jiang, S. (2016). FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients. Experimental and Therapeutic Medicine, 12, 2753-2758. https://doi.org/10.3892/etm.2016.3662
MLA
Zhang, J., Chen, X., Liu, T., Jiang, S."FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients". Experimental and Therapeutic Medicine 12.4 (2016): 2753-2758.
Chicago
Zhang, J., Chen, X., Liu, T., Jiang, S."FOXP3+ associated with the pro-inflammatory regulatory T and T helper 17 effector cells in asthma patients". Experimental and Therapeutic Medicine 12, no. 4 (2016): 2753-2758. https://doi.org/10.3892/etm.2016.3662
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