IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v510y2014i7505d10.1038_nature13444.html
   My bibliography  Save this article

Inactivation of PI(3)K p110δ breaks regulatory T-cell-mediated immune tolerance to cancer

Author

Listed:
  • Khaled Ali

    (UCL Cancer Institute, Paul O’Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK
    Present Addresses: Oncology Research, Amgen, 1120 Veterans Boulevard, South San Francisco, California 94080, USA (K.A.); University of Birmingham, School of Infection and Immunity, Centre for Translational Inflammation Research, New Queen Elizabeth Hospital Research Laboratory, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, UK (D.R.S.).)

  • Dalya R. Soond

    (Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK
    Present Addresses: Oncology Research, Amgen, 1120 Veterans Boulevard, South San Francisco, California 94080, USA (K.A.); University of Birmingham, School of Infection and Immunity, Centre for Translational Inflammation Research, New Queen Elizabeth Hospital Research Laboratory, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, UK (D.R.S.).)

  • Roberto Piñeiro

    (UCL Cancer Institute, Paul O’Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK)

  • Thorsten Hagemann

    (Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK)

  • Wayne Pearce

    (UCL Cancer Institute, Paul O’Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK)

  • Ee Lyn Lim

    (Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK)

  • Hicham Bouabe

    (Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK)

  • Cheryl L. Scudamore

    (Mary Lyon Centre, MRC Harwell, Harwell Science and Innovation Campus, Harwell OX11 0RD, UK)

  • Timothy Hancox

    (Piramed Pharma, 957 Buckingham Avenue, Slough, Berkshire SL1 4NL, UK)

  • Heather Maecker

    (Cancer Signaling and Translational Oncology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080-4990, USA)

  • Lori Friedman

    (Cancer Signaling and Translational Oncology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080-4990, USA)

  • Martin Turner

    (Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK)

  • Klaus Okkenhaug

    (Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK)

  • Bart Vanhaesebroeck

    (UCL Cancer Institute, Paul O’Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK)

Abstract

The kinase PI(3)Kδ is shown to be required for the immunosuppressive function of regulatory T cells; inactivation of PI(3)Kδ in these cells leads to enhanced cytotoxic T-cell function and restricts tumour growth and metastasis in a variety of mouse tumour models.

Suggested Citation

  • Khaled Ali & Dalya R. Soond & Roberto Piñeiro & Thorsten Hagemann & Wayne Pearce & Ee Lyn Lim & Hicham Bouabe & Cheryl L. Scudamore & Timothy Hancox & Heather Maecker & Lori Friedman & Martin Turner &, 2014. "Inactivation of PI(3)K p110δ breaks regulatory T-cell-mediated immune tolerance to cancer," Nature, Nature, vol. 510(7505), pages 407-411, June.
    • Handle: RePEc:nat:nature:v:510:y:2014:i:7505:d:10.1038_nature13444
    DOI: 10.1038/nature13444
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature13444
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature13444?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
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

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


    Cited by:

    1. Sardanyés, Josep & Rodrigues, Carla & Januário, Cristina & Martins, Nuno & Gil-Gómez, Gabriel & Duarte, Jorge, 2015. "Activation of effector immune cells promotes tumor stochastic extinction: A homotopy analysis approach," Applied Mathematics and Computation, Elsevier, vol. 252(C), pages 484-495.

    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:nature:v:510:y:2014:i:7505:d:10.1038_nature13444. 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.