A novel model for dissecting roles of IL-17 in lung transplantation

Lung transplantation is the final therapeutic option for patients with end-stage lung disease. However, chronic lung allograft dysfunction (CLAD), classified as azithromycin reversible allograft dysfunction (ARAD), bronchiolitis obliterans syndrome (BOS), and restrictive allograft syndrome (RAS), is the major cause of low long-term survival rates for those patients after lung transplantation (1). Fifty percent primary adult lung transplant recipients developed acute cellular rejection, which has been conformed to be associated with BOS and RAS (2). IL-17 is now recognized to play important roles in the development of CLAD (3), while the precise cellular and molecular mechanisms governing these processes remain to be explored