Background The IL-23/Th17 pathway plays an important role in the development of chronic inflammatory diseases and autoimmune diseases. However, the role of the IL-23/Th17 axis in the regulation of virus myocarditis (VMC) is still largely unknown.
Methods VMC was induced in male Balb/c mice by CVB3 peritoneal injection. Mice injected with PBS were taken as the controls. IL-23, IL-17 and RORγt mRNA in the myocardium of VMC were assessed by semi-quantitative RT-PCR on the time of 0, 1, 2, 3, 4 and 6 weeks after injection. IL-23, IL-17 protein from blood plasma was evaluated by ELISA. Flow cytometric analysis was used to evaluate the frequencies of Th17 subsets in CD4+Tcell. CD4+ T cells were isolated from VMC mice and cultured with rIL-23 in vitro to investigate the function of IL-23 in the IL-23/Th-17 pathway.
Results Comparing with the controls, IL-23, IL-17 and RORγt mRNA were steadily expressed in the myocardium of infected mice from 1 week after virus injection (p<0.01), IL-23 and IL17 protein level increased from 1st week to 6th week. The frequencies of Th17 cells were obviously increased in VMC mice 1 week after infection (p<0.01), the maximum level of Th17 cells was reached at 4th week. The ratio of Th17 cells in the spleen lymphocyte significantly improved after rIL-23 stimulation, the IL-17 and RORγt mRNA expression of the cultured cells and the IL-17 protein in the culture supernatants increased after rIL-23 stimulation (p<0.05).
Conclusions IL-23/Th-17 pathway may play an essential role in VMC.