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Nat Commun. 2016 Mar 11;7:10928. doi: 10.1038/ncomms10928.

IL-17-producing γδ T cells enhance bone regeneration.

Author information

1
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.
2
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.
3
Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan.
4
Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency (JST), Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan.
5
Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology (AMED-CREST), Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan.
6
Laboratory for Immune Homeostasis, RIKEN Center for Integrative Medical Science, Suehiro-cho 1-7-22, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
7
Research Institute for Biological Sciences, Tokyo University of Science, Yamazaki 2669, Noda, Chiba 278-0022, Japan.

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.

PMID:
26965320
PMCID:
PMC4792964
DOI:
10.1038/ncomms10928
[Indexed for MEDLINE]
Free PMC Article

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