OBJECTIVE: Allergic asthma is a chronic airway inflammation resulting from an imbalance of T helper (Th) cell responses to allergens. Interleukin (IL)-35 has been shown to have potent immunoregulatory properties. Whether IL-35 participates in the immunopathogenesis of allergic asthma patients is still unknown. METHODS: CD4+ T cells and CD4+ CD25- T cells were obtained from peripheral blood mononuclear cells (PBMCs) using magnetic separation. The concentration of IL-35 in plasma was measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of the IL-35 subunits, EBI3 and IL-12p35, were detected by quantitative real-time PCR (qPCR). The proliferative responses of CFSE-labeled CD4+ CD25- T cells in the presence or absence of rhIL-35 were evaluated by flow cytometry. Cytokine production of activated CD4+ CD25- T cells was examined by flow cytometry and ELISA. RESULTS: IL-35 protein and mRNA levels were decreased in allergic asthmatics. The frequencies of CD4+ CD25+ Foxp3+ Tregs and CD4+ IL-12p35+ T cells in allergic asthma patients were lower than in healthy controls. Moreover, the addition of rhIL-35 suppressed CFSE+ CD4+ CD25- T cell proliferation in vitro in a dose-dependent manner, and the suppression induced by rhIL-35 was associated with decreases in IL-4 but not IFN-γ and IL-17 production of activated CD4+ CD25- T cells. The increased level of Th1/Th2 was observed in allergic asthmatics in the presence of rhIL-35. CONCLUSIONS: Our data suggest that IL-35 can effectively suppress the proliferation and IL-4 production of activated CD4+ CD25- T cells in allergic asthma, and that IL-35 may be a new immunotherapy for asthma patients.
OBJECTIVE:Allergic asthma is a chronic airway inflammation resulting from an imbalance of T helper (Th) cell responses to allergens. Interleukin (IL)-35 has been shown to have potent immunoregulatory properties. Whether IL-35 participates in the immunopathogenesis of allergic asthmapatients is still unknown. METHODS:CD4+ T cells and CD4+ CD25- T cells were obtained from peripheral blood mononuclear cells (PBMCs) using magnetic separation. The concentration of IL-35 in plasma was measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of the IL-35 subunits, EBI3 and IL-12p35, were detected by quantitative real-time PCR (qPCR). The proliferative responses of CFSE-labeled CD4+ CD25- T cells in the presence or absence of rhIL-35 were evaluated by flow cytometry. Cytokine production of activated CD4+ CD25- T cells was examined by flow cytometry and ELISA. RESULTS: IL-35 protein and mRNA levels were decreased in allergic asthmatics. The frequencies of CD4+ CD25+ Foxp3+ Tregs and CD4+ IL-12p35+ T cells in allergic asthmapatients were lower than in healthy controls. Moreover, the addition of rhIL-35 suppressed CFSE+ CD4+ CD25- T cell proliferation in vitro in a dose-dependent manner, and the suppression induced by rhIL-35 was associated with decreases in IL-4 but not IFN-γ and IL-17 production of activated CD4+ CD25- T cells. The increased level of Th1/Th2 was observed in allergic asthmatics in the presence of rhIL-35. CONCLUSIONS: Our data suggest that IL-35 can effectively suppress the proliferation and IL-4 production of activated CD4+ CD25- T cells in allergic asthma, and that IL-35 may be a new immunotherapy for asthmapatients.
Entities:
Keywords:
Allergic asthma; CD4+CD25− T cells; IL-35; IL-4, proliferative responses
Authors: Yi Li; Yihao Wang; Hui Liu; Kai Ding; Shanfeng Hao; Yuanyuan Shao; Honglei Wang; Jin Chen; Lei Huang; Zonghong Shao; Rong Fu Journal: Mol Med Rep Date: 2017-12-11 Impact factor: 2.952
Authors: P Bayrak Degirmenci; S Aksun; Z Altin; F Bilgir; I B Arslan; H Colak; B Ural; D Solakoglu Kahraman; G Diniz; B Ozdemir; C Kırmaz Journal: Dis Markers Date: 2018-03-06 Impact factor: 3.434