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Host defense against oral microbiota by bone-damaging T cells

Author

Listed:
  • Masayuki Tsukasaki

    (The University of Tokyo)

  • Noriko Komatsu

    (The University of Tokyo)

  • Kazuki Nagashima

    (The University of Tokyo)

  • Takeshi Nitta

    (The University of Tokyo)

  • Warunee Pluemsakunthai

    (The University of Tokyo)

  • Chisa Shukunami

    (Hiroshima University)

  • Yoichiro Iwakura

    (Tokyo University of Science)

  • Tomoki Nakashima

    (Tokyo Medical and Dental University
    Precursory Research for Embryonic Science and Technology (PRESTO)
    Core Research for Evolutional Science and Technology (AMED-CREST))

  • Kazuo Okamoto

    (The University of Tokyo)

  • Hiroshi Takayanagi

    (The University of Tokyo)

Abstract

The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic TH17 cells induce bone destruction and autoimmune inflammation. However, whether a beneficial function of T-cell-induced bone damage exists is unclear. Here, we show that bone-damaging T cells have a critical function in the eradication of bacteria in a mouse model of periodontitis, which is the most common infectious disease. Bacterial invasion leads to the generation of specialized TH17 cells that protect against bacteria by evoking mucosal immune responses as well as inducing bone damage, the latter of which also inhibits infection by removing the tooth. Thus, bone-damaging T cells, which may have developed to stop local infection by inducing tooth loss, function as a double-edged sword by protecting against pathogens while also inducing skeletal tissue degradation.

Suggested Citation

  • Masayuki Tsukasaki & Noriko Komatsu & Kazuki Nagashima & Takeshi Nitta & Warunee Pluemsakunthai & Chisa Shukunami & Yoichiro Iwakura & Tomoki Nakashima & Kazuo Okamoto & Hiroshi Takayanagi, 2018. "Host defense against oral microbiota by bone-damaging T cells," Nature Communications, Nature, vol. 9(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03147-6
    DOI: 10.1038/s41467-018-03147-6
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    Cited by:

    1. Anhao Liu & Mikihito Hayashi & Yujin Ohsugi & Sayaka Katagiri & Shizuo Akira & Takanori Iwata & Tomoki Nakashima, 2024. "The IL-33/ST2 axis is protective against acute inflammation during the course of periodontitis," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. Masayuki Tsukasaki & Noriko Komatsu & Takako Negishi-Koga & Nam Cong-Nhat Huynh & Ryunosuke Muro & Yutaro Ando & Yuka Seki & Asuka Terashima & Warunee Pluemsakunthai & Takeshi Nitta & Takashi Nakamura, 2022. "Periosteal stem cells control growth plate stem cells during postnatal skeletal growth," Nature Communications, Nature, vol. 13(1), pages 1-11, December.
    3. Tetsuya Yoshimoto & Mizuho Kittaka & Andrew Anh Phuong Doan & Rina Urata & Matthew Prideaux & Roxana E. Rojas & Clifford V. Harding & W. Henry Boom & Lynda F. Bonewald & Edward M. Greenfield & Yasuyos, 2022. "Osteocytes directly regulate osteolysis via MYD88 signaling in bacterial bone infection," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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