Skewed balance of regulatory T cell and inflammatory T cell in IL-17 defect with human metapneumovirus infection

Abstract

Human metapneumovirus (hMPV) is a common cause of respiratory infections in children. However, the precise mechanisms underlying the development of hMPV-induced pulmonary pathology remain unknown. Studies show that IL-17 plays an important role in some inflammatory diseases of the airways, including asthma and chronic obstructive pulmonary disease. Here, we generated an IL-17 KO murine model of hMPV infection and used it to characterize the role of IL-17 hMPV-induced pulmonary inflammation. The results demonstrated that the defect in IL-17 resulted in less neutrophil influx into the lungs, along with reduced ventilatory function. Meanwhile, viral infection in IL-17 KO mice increased regulatory T cells (Tregs) and reduced Th1 and Th2 cells in the lung, suggesting that lack of IL-17 skews the immune response in the lung toward an anti-inflammatory profile, as exhibited by a greater number of Treg cells and fewer Th1 and Th2 cells.