Ono Takehito, Okamoto Kazuo, Nakashima Tomoki, Nitta Takeshi, Hori Shohei, Iwakura Yoichiro, Takayanagi Hiroshi
Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.
Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Program, Takayanagi Osteonetwork Project, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.
Nat Commun. 2016 Mar 11;7:10928. doi: 10.1038/ncomms10928.
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.
免疫反应不仅对宿主抵御病原体至关重要，而且对损伤后的组织维持和修复也很关键。淋巴细胞参与组织损伤后的愈合过程，包括骨折和肌肉损伤。然而，愈合过程中具体的免疫细胞亚群和介质尚不完全清楚。在此，我们表明γδ T细胞产生IL-17A，其促进骨形成并促进骨折愈合。由于成骨细胞骨形成缺陷，IL-17A缺陷小鼠的修复受损。IL-17A通过刺激间充质祖细胞的增殖和成骨细胞分化来加速骨形成。本研究确定了产生IL-17的γδ T细胞在骨骼组织再生中的新作用。
