Halofuginone treatment reduces interleukin-17A and ameliorates features of chronic lung allograft dysfunction in a mouse orthotopic lung transplant model

摘要: Background Increasing evidence suggests that interleukin (IL)-17A plays an important role in chronic lung allograft dysfunction (CLAD), characterized by airway and parenchymal fibrosis, after transplantation. Halofuginone is a plant derivative has been shown to inhibit Th17 differentiation. The purpose of this study was examine the effect halofuginone on CLAD development using minor alloantigen‒mismatched mouse orthotopic transplant model. Methods C57BL/6 recipient mice received left from C57BL/10 donors, mismatched for antigens. Lung recipients daily intraperitoneal injections 2.5 μg or vehicle alone. grafts were assessed Days 7, 14, 28 post-transplant. Results Compared with control mice, Day post-transplant, treated showed significant reduction percentage obliterated airways (6.8 ± 4.7% vs 52.5 13.8%, p Conclusion beneficial fibrosis model highlights IL-17A merits further pre-clinical clinical studies.