Abstract
Objective:
Natural killer cells play immunomodulatory role the pathogenesis of chronic inflammatory airway diseases. NK cells may induce allergic airway inflammation by increasing the production of type 2 cytokines.
Materials and Methods:
Intracytoplasmic cytokine levels of IL-13, IL-4, IFN-γ and IL-10 in NK cells and plasma levels of IFN-γ, TNF-α, IL-2, IL-8, IL-4, IL-5, IL-6, IL-17, IL12, IL-13, IL-1β and IL-10 in patients with newly diagnosed asthma, asthmatic patients under treatment and controls by using flow cytometry and ProcartaPlex multiplex immunoassays kit were measured.
Results:
The numbers of IFN-γ+ NK1 cells were decreased in both patient groups; comparing both asthmatic groups, IFN-γ+ NK1 cells were higher in asthmatic patients under treatment. Intracellular IL-4 levels of NK cells were increased, however IL-10+ NK cells were diminished in both patient groups vs. controls. Increased number of IL-13+ NK2 cells in newly-diagnosed asthmatics vs. asthmatics patients under treatment and controls were obtained. Increased levels of plasma IL-1β levels in newly- diagnosed asthmatic patients compared to that of asthmatics under treatment were found. Newly-diagnosed asthmatics showed higher IL-8 levels compared to asthmatics under treatment and controls. Increased IL-5 levels were measured in newly-diagnosed asthmatic patients compared to healthy subjects and higher IL-13 levels were detected in newly-diagnosed asthmatic patients vs. other groups and also in controls vs. patients with asthma patients under treatment. IL-10 and IL-12 levels were decreased in newly- diagnosed asthmatic patients compared to healthy subjects. Compared to healthy subjects in both asthmatic patients’ also diminished IL-2 levels were obtained.
Conclusion:
In order to use NK cells as a therapeutic target, a strategy must be established to regulate its cytokine secretion functions with respect to their role of these cells in each disease.
Keywords:
Asthma, flow cytometry, natural killer cells, cytokinesVOLUME
,
ISSUE
Correspondence
Received
Accepted
Published
Suggested Citation
DOI
License