Abstract
Immune responses are crucial not only for host defence against pathogens but also for tissue maintenance and repair after injury. Lymphocytes are involved in the healing process after tissue injury, including bone fracture and muscle damage. However, the specific immune cell subsets and mediators of healing are not entirely clear. Here we show that γδ T cells produce IL-17A, which promotes bone formation and facilitates bone fracture healing. Repair is impaired in IL-17A-deficient mice due to a defect in osteoblastic bone formation. IL-17A accelerates bone formation by stimulating the proliferation and osteoblastic differentiation of mesenchymal progenitor cells. This study identifies a novel role for IL-17-producing γδ T cells in skeletal tissue regeneration.
Highlights
Immune responses are crucial for host defence against pathogens and for tissue maintenance and repair after injury
These results suggest that IL-17A promotes bone regeneration by activating osteoblastic bone formation without affecting osteoclastic bone resorption
We reveal that Vg6 þ gd T cells (T cell receptor (TCR) nomenclature of Heilig and Tonegawa)[12] proliferate in the injury site and function as the crucial producer of IL-17A in fracture healing
Summary
Immune responses are crucial for host defence against pathogens and for tissue maintenance and repair after injury. Lymphocytes are involved in the healing process after tissue injury, including bone fracture and muscle damage. Repair is impaired in IL-17A-deficient mice due to a defect in osteoblastic bone formation. This study identifies a novel role for IL-17-producing gd T cells in skeletal tissue regeneration. Il17a / mice than in the wild-type mice (Fig. 2c,d). It has been suggested that IL-17F is involved in fracture repair[8], there was no significant difference in bone regeneration in the wild-type and Il17f / mice (Supplementary Fig. 1f–i). New bone was formed as trabecula-like structures in the drill hole in both the wild-type and Il17a / mice (Fig. 2e). The ratio of the cuboidal osteoblast surface to the bone surface was lower in the Il17a /
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