IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-01687-x.html
   My bibliography  Save this article

TLR7 mediated viral recognition results in focal type I interferon secretion by dendritic cells

Author

Listed:
  • Shin-Ichiroh Saitoh

    (The Institute of Medical Science, The University of Tokyo)

  • Fumiko Abe

    (The University of Tokyo)

  • Atsuo Kanno

    (The Institute of Medical Science, The University of Tokyo)

  • Natsuko Tanimura

    (The Institute of Medical Science, The University of Tokyo)

  • Yoshiko Mori Saitoh

    (The Institute of Medical Science, The University of Tokyo)

  • Ryutaro Fukui

    (The Institute of Medical Science, The University of Tokyo)

  • Takuma Shibata

    (The Institute of Medical Science, The University of Tokyo)

  • Katsuaki Sato

    (University of Miyazaki)

  • Takeshi Ichinohe

    (The University of Tokyo)

  • Mayumi Hayashi

    (Ltd., 1-16-13 Kitakasai)

  • Kazuishi Kubota

    (Ltd., 1-16-13 Kitakasai)

  • Hiroko Kozuka-Hata

    (The University of Tokyo)

  • Masaaki Oyama

    (The University of Tokyo)

  • Yorifumi Kikko

    (The University of Tokyo)

  • Toshiaki Katada

    (The University of Tokyo)

  • Kenji Kontani

    (The University of Tokyo
    Meiji Pharmaceutical University)

  • Kensuke Miyake

    (The Institute of Medical Science, The University of Tokyo
    The Institute of Medical Science, The University of Tokyo)

Abstract

Plasmacytoid dendritic cells (pDC) sense viral RNA through toll-like receptor 7 (TLR7), form self-adhesive pDC–pDC clusters, and produce type I interferons. This cell adhesion enhances type I interferon production, but little is known about the underlying mechanisms. Here we show that MyD88-dependent TLR7 signaling activates CD11a/CD18 integrin to induce microtubule elongation. TLR7+ lysosomes then become linked with these microtubules through the GTPase Arl8b and its effector SKIP/Plekhm2, resulting in perinuclear to peripheral relocalization of TLR7. The type I interferon signaling molecules TRAF3, IKKα, and mTORC1 are constitutively associated in pDCs. TLR7 localizes to mTORC1 and induces association of TRAF3 with the upstream molecule TRAF6. Finally, type I interferons are secreted in the vicinity of cell–cell contacts between clustered pDCs. These results suggest that TLR7 needs to move to the cell periphery to induce robust type I interferon responses in pDCs.

Suggested Citation

  • Shin-Ichiroh Saitoh & Fumiko Abe & Atsuo Kanno & Natsuko Tanimura & Yoshiko Mori Saitoh & Ryutaro Fukui & Takuma Shibata & Katsuaki Sato & Takeshi Ichinohe & Mayumi Hayashi & Kazuishi Kubota & Hiroko , 2017. "TLR7 mediated viral recognition results in focal type I interferon secretion by dendritic cells," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01687-x
    DOI: 10.1038/s41467-017-01687-x
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-01687-x
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-017-01687-x?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Manon Venet & Margarida Sa Ribeiro & Elodie Décembre & Alicia Bellomo & Garima Joshi & Célia Nuovo & Marine Villard & David Cluet & Magali Perret & Rémi Pescamona & Helena Paidassi & Thierry Walzer & , 2023. "Severe COVID-19 patients have impaired plasmacytoid dendritic cell-mediated control of SARS-CoV-2," Nature Communications, Nature, vol. 14(1), pages 1-21, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01687-x. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.