Abstract
BackgroundThe differentiation of CD4+ lymphocytes Th17/regulatory T cells (Treg) and indoleamine 2,3-dioxygenase (IDO) is associated with the pathogenesis of allergic asthma. Basic research has shown that IDO is likely a “switch” of the transition from Th17 cells to Tregs under certain conditions. However, no relevant clinical studies have been reported on the association between IDO activity and Th17/Treg imbalance in children with allergic asthma. The goal of this study was to test whether indoleamine 2,3 dioxygenase (IDO) participates in the pathogenesis of pediatric allergic asthma by influencing Th17/regulatory T cell (Treg) differentiation and related cytokines.MethodsThirty-three children with allergic asthma and 33 healthy children were selected. The subjects were evaluated via a pulmonary function test, a skin prick test, and an eosinophil count. Peripheral blood was collected to measure Th17/Treg percentages and related cytokine levels. Blood and induced sputum were obtained to measure the IDO level.ResultsCompared with the control group, the patient group had an obvious Th17/Treg imbalance; their IDO levels were significantly lower, their IL-17 and IL-6 levels were markedly higher, and their IL-10 and TGF-β levels were markedly lower than those of the control group. The IDO levels in both blood and induced sputum were negatively correlated with the Th17/Treg ratio.ConclusionsA significant correlation was observed between IDO activity and Th17/Treg imbalance in children with allergic asthma. IDO may upregulate Treg numbers by stimulating IL-10 production and inhibiting IL-6 expression. Therefore, IDO may be a molecular switch that leads to the conversion of Th17 cells to Tregs, thus playing a potentially protective role in the pathogenesis of asthma.Trial registration This study was approved by the Chinese Clinical Trial Registry with registration number ChiCTR-COC-15006080 and was reviewed and approved by the Ethics Committee of Southwest Hospital. The name of registration: The effect of indoleamine 2,3 dioxygenase (IDO) on Regulation of Th17/Treg Differentiation in Childhood Asthma. Date of registration: 14/03/2015. URL of trial registry record: http://www.chictr.org.cn
Highlights
The differentiation of CD4+ lymphocytes Th17/regulatory T cells (Treg) and indoleamine 2,3-dioxygenase (IDO) is associated with the pathogenesis of allergic asthma
This study investigated the association between IDO activity and Th17/Treg expression and the possible molecular mechanisms in pediatric patients older than 5 years with allergic asthma compared with children without any allergic symptoms
This study found significantly reduced IDO expression in the peripheral blood and induced sputum of children with allergic asthma compared to healthy children matched by age and gender, suggesting that IDO activity can inhibit airway allergic reactions and has a protective effect in the pathogenic mechanism of pediatric allergic asthma
Summary
The differentiation of CD4+ lymphocytes Th17/regulatory T cells (Treg) and indoleamine 2,3-dioxygenase (IDO) is associated with the pathogenesis of allergic asthma. No relevant clinical studies have been reported on the association between IDO activity and Th17/Treg imbalance in children with allergic asthma. The goal of this study was to test whether indoleamine 2,3 dioxygenase (IDO) participates in the pathogenesis of pediatric allergic asthma by influencing Th17/regulatory T cell (Treg) differentiation and related cytokines. Studies in animal models have demonstrated that the ability of Tregs to inhibit the inflammatory response of Th2 cells is key to the development of tolerance to asthma. Zhao et al [3] demonstrated in a chronic airway inflammation model that Th17 cells inhibit Treg-mediated tolerance and concluded that chronic airway inflammation could be improved through regulation of the Th17/Treg axis
Sign-in/Register to view highlights & summary 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.
