IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-00573-w.html
   My bibliography  Save this article

Signalling strength determines proapoptotic functions of STING

Author

Listed:
  • Muhammet F. Gulen

    (Ecole Polytechnique Fédérale de Lausanne (EPFL))

  • Ute Koch

    (Ecole Polytechnique Fédérale de Lausanne (EPFL))

  • Simone M. Haag

    (Ecole Polytechnique Fédérale de Lausanne (EPFL))

  • Fabian Schuler

    (Medical University of Innsbruck)

  • Lionel Apetoh

    (Université de Bourgogne)

  • Andreas Villunger

    (Medical University of Innsbruck
    Tyrolean Cancer Research Institute)

  • Freddy Radtke

    (Ecole Polytechnique Fédérale de Lausanne (EPFL))

  • Andrea Ablasser

    (Ecole Polytechnique Fédérale de Lausanne (EPFL))

Abstract

Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prevents in vivo growth of T-cell-derived tumours independent of its adjuvant activity. Our results demonstrate how the magnitude of STING signalling can shape distinct effector responses, which may permit for cell type-adjusted behaviours towards endogenous or exogenous insults.

Suggested Citation

  • Muhammet F. Gulen & Ute Koch & Simone M. Haag & Fabian Schuler & Lionel Apetoh & Andreas Villunger & Freddy Radtke & Andrea Ablasser, 2017. "Signalling strength determines proapoptotic functions of STING," Nature Communications, Nature, vol. 8(1), pages 1-10, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00573-w
    DOI: 10.1038/s41467-017-00573-w
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-00573-w
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-017-00573-w?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. Matteo Gentili & Bingxu Liu & Malvina Papanastasiou & Deborah Dele-Oni & Marc A. Schwartz & Rebecca J. Carlson & Aziz M. Al’Khafaji & Karsten Krug & Adam Brown & John G. Doench & Steven A. Carr & Nir , 2023. "ESCRT-dependent STING degradation inhibits steady-state and cGAMP-induced signalling," Nature Communications, Nature, vol. 14(1), pages 1-22, December.
    2. Chiara Scopa & Samantha M. Barnada & Maria E. Cicardi & Mo Singer & Davide Trotti & Marco Trizzino, 2023. "JUN upregulation drives aberrant transposable element mobilization, associated innate immune response, and impaired neurogenesis in Alzheimer’s disease," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    3. Jeremy J. Ratiu & William E. Barclay & Elliot Lin & Qun Wang & Sebastian Wellford & Naren Mehta & Melissa J. Harnois & Devon DiPalma & Sumedha Roy & Alejandra V. Contreras & Mari L. Shinohara & David , 2022. "Loss of Zfp335 triggers cGAS/STING-dependent apoptosis of post-β selection thymocytes," Nature Communications, Nature, vol. 13(1), pages 1-18, 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_s41467-017-00573-w. 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.