Abstract
Objective. Allergic asthma is a common inflammatory disease regulated by the T helper (Th) cells. Interferon regulatory factor 4 (IRF4) plays an important role in the differentiation of Th cells. This study investigated whether IRF4 is involved in the systemic immune responses in allergic asthma patients. Methods. Peripheral blood mononuclear cells (PBMCs) were isolated from allergic asthmatics (n = 29) and healthy controls (n = 12). The mRNA and protein levels of IRF4 in PBMCs were measured by quantitative RT-PCR and western blotting. The frequencies of Th1, Th2, and Th17 cells were analyzed by flow cytometry. The related cytokine (interferon-γ, interleukin-4 (IL-4), and IL-17) concentrations in plasma and culture supernatants were measured by ELISA. The levels of GATA binding protein 3 (GATA3), retinoic acid-related orphan receptor γt (RORγt), and forkhead box P3 (FOXP3), the master transcription factors controlling Th2, Th17, and T regulatory cells differentiation, respectively, were examined by quantitative RT-PCR. Results. The levels of IRF4 were elevated in allergic asthmatics compared with those in healthy controls. The frequencies of Th2 and Th17 cells as well as the concentrations of Th2- and Th17-related cytokines were higher in plasma from asthma patients than those from healthy controls; similar results were observed in culture supernatants. IRF4 mRNA levels were positively correlated with GATA3, RORγt, and FOXP3 mRNA levels in allergic asthmatics but not in healthy controls. Conclusions. Our results suggested that IRF4 may play a role in the systemic inflammation of allergic asthma patients by facilitating the differentiation of Th2 and Th17 cells at least at the transcriptional level.
Acknowledgements
The authors thank Dr. Yu-hui Lin and Dr. Wei-min Liu (Zhongnan Hospital of Wuhan University) for recruiting allergic asthma patients.
Declaration of Interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. This work was supported by NSFC (30871122, to Yang J) and the Fundamental Research Funds for the Central Universities (to Chen X).