Posted at the Institutional Resources for Unique Collection and Academic Archives at Tokyo Dental College, Available from http://ir.tdc.ac.jp/
Title
Periodontitis, arthritis and osteoimmunology
Author(s)
Hiroshi, Takayanagi
Journal
歯科学報, 119(5): 435-436
URL
http://hdl.handle.net/10130/5028
Right
Osteoimmunology deals with the interaction and shared mechanisms of the bone and the immune system, and is important for understanding the pathology of bone destruction associated with inflammation. T cells represent the cells that control the adaptive immune system by eradicating the infected cells as well as helping B cells to generate antibodies. On the other hand, T cells play a crucial role in the bone damage as-sociated with activated or prolonged immune responses in autoimmunity and infection. We characterized the T cells responsible for such inflammation-associated bone damage and discovered that Th 17 cells are the major bone-damaging subset. Bone-damaging T cells greatly contribute to both autoimmune inflamma-tion and bone destrucinflamma-tion in the context of autoimmune arthritis. However, it is very difficult to find a bene-ficial function of bone-damaging T cells. IL-１７ and Th 17 cells are known to play an important role in the host defense against bacteria by inducing anti-bacterial peptides, recruiting neutrophils and promoting local inflammation through cytokines and chemokines. We explored the role of bone-damaging T cells in the peri-odontitis. Th１７ cells stimulate the antibacterial responses and at the same time promotes osteoclastic bone destruction via the induction of RANK, leading to the resolution of infection and inflammation by removing the infected-tooth. Thus, we propose that bone-damaging T cells, which may have developed to stop local infection by inducing tooth loss, function like a double-edged sword by protecting against pathogens while also inducing skeletal tissue degradation. Here I will review the recent advance in the field of osteoimmu-nology and its relevance in bone loss associated with inflammation as well as other physiological and patho-logical conditions.
２０１９ International Symposium
Tokyo Dental College Research Branding Project
Periodontitis, arthritis and osteoimmunology
Hiroshi Takayanagi, MD, PhD
Professor
Department of Immunology
Graduate School of Medicine and Faculty of Medicine
The University of Tokyo
Session２：Molecular and cellular mechanism of periodontitis and its application to development of new therapy
歯科学報 Vol．１１９，No．５（２０１９） ４３５
Curriculum Vitae
１９８６−１９９０ Faculty of Medicine, The University of Tokyo, MD．
１９９６−１９９７ Department of Orthopaedic Surgery, the University of Tokyo Hospital． １９９７−２００１ Graduate School of Medicine, The University of Tokyo, PhD.
２００１−２００３ Research Associate, Department of Immunology, Graduate School of Medicine, The Univer-sity of Tokyo．
２００３−２００５ Project Professor, Department of Cellular Physiological Chemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University．
２００５−２０１２ Professor, Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University．
２００９−２０１５ Research Director of Takayanagi Osteonetwork Project, the Exploratory Research for Advanced Technology（ERATO）research funding program provided by Japan Science and Technology Agency（JST）．
２０１２−Current Professor, Department of Immunology, Graduate School of Medicine and Faculty of Medi-cine, The University of Tokyo．
Research Fields of Interest
Osteoimmunology, Immune Tolerance, Arthritis．
Selected Pulications
１．Hayashi M, Nakashima T, Taniguchi M, Kodama T, Kumanogoh A, Takayanagi H：Osteoprotection by semaphoring ３A. Nature. ４８５，６９０７４，２０１２．
２．Komatsu N, Okamoto K, Sawa S, Nakashima T, Oh-hora M, Kodama T, Tanaka S, Bluestone JA, Takay-anagi H：Pathogenic conversion of Foxp３＋ T cells into TH 17 cells in autoimmune arthritis. Nat Med. ２０，６２−８，２０１４．
３．Takaba H, Morishita Y, Tomofuji Y, Danks L, Nitta T, Komatsu N, Kodama T, Takayanagi H：Fezf２ Orchestrates a Thymic Program of Self-Antigen Expression for Immune Tolerance. Cell. １６３, ９７５− ９８７，２０１５．
４．Guerrini MM, Okamoto K, Komatsu N, Sawa S, Danks L, Penninger JM, Nakashima T, Takayanagi H： Inhibition of the TNF Family Cytokine RANKL Prevents Autoimmune Inflammation in the Central Nerv-ous System. Immunity. ４３，１１７４−８５，２０１５．
５．Terashima A, Okamoto K, Nakashima T, Akira S, Ikuta K, Takayanagi H：Sepsis-Induced Osteoblast Ablation Causes Immunodeficiency. Immunity. ４４，１４３４−４３，２０１６．
６．Nagashima K, Sawa S, Nitta T, Tsutsumi M, Okamura T, Penninger JM, Nakashima T, Takayanagi H： Identification of subepithelial mesenchymal cells that induce IgA and diversify gut microbiota. Nat Immu-nol.１８，６７５−６８２，２０１７．
７．Inoue M, Okamoto K, Terashima A, Nitta T, Muro R, Negishi-Koga T, Kitamura T, Nakashima T, Takayanagi H：Arginine methylation controls the strength ofγc-family cytokine signaling in T cell main-tenance. Nat Immunol. １９，１２６５−１２７６，２０１８．
８．Hayashi M, Nakashima T, Yoshimura N, Okamoto K, Tanaka S, Takayanagi H：Autoregulation of Os-teocyte Sema３A Orchestrates Estrogen Action and Counteracts Bone Aging. Cell Met. ２９，１−１１， ２０１９．
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