IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v467y2010i7312d10.1038_nature09337.html
   My bibliography  Save this article

A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells

Author

Listed:
  • Nicolas Manel

    (Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
    CNRS-UMR5535, Institut de Génétique Moléculaire de Montpellier, Université Montpellier I and II)

  • Brandon Hogstad

    (Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
    Howard Hughes Medical Institute, New York University School of Medicine)

  • Yaming Wang

    (New York University School of Medicine)

  • David E. Levy

    (New York University School of Medicine)

  • Derya Unutmaz

    (New York University School of Medicine)

  • Dan R. Littman

    (Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
    Howard Hughes Medical Institute, New York University School of Medicine
    New York University School of Medicine)

Abstract

HIV-1 in dendritic cells HIV-1 (human immunodeficiency virus 1) infection fails to induce interferon in the cells that it infects, but the underlying mechanisms involved are undefined. Dendritic cells — immune cells found in skin, mucosa and lymph tissues — mediate the innate detection of pathogens and the activation of other immune cells involved in specific adaptive immunity. But not for HIV. Dendritic cells are resistant to infection by HIV, although they do bind to the virus and are thought to facilitate the infection of T-helper cells. Now it is shown that when the usual block to HIV infection is bypassed in dendritic cells — by exposure to the Vpx accessory protein from the simian immunodeficiency virus SIVmac — HIV does induce a type I interferon response and T-cell activation. The virulence of HIV-1 may be related to its ability to evade innate immunity by staying out of dendritic cells, and the manipulation of that strategy may be of relevance to vaccine design.

Suggested Citation

  • Nicolas Manel & Brandon Hogstad & Yaming Wang & David E. Levy & Derya Unutmaz & Dan R. Littman, 2010. "A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells," Nature, Nature, vol. 467(7312), pages 214-217, September.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7312:d:10.1038_nature09337
    DOI: 10.1038/nature09337
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature09337
    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/nature09337?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. Caroline Passaes & Delphine Desjardins & Anaïs Chapel & Valérie Monceaux & Julien Lemaitre & Adeline Mélard & Federico Perdomo-Celis & Cyril Planchais & Maël Gourvès & Nastasia Dimant & Annie David & , 2024. "Early antiretroviral therapy favors post-treatment SIV control associated with the expansion of enhanced memory CD8+ T-cells," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    2. Lisa D. J. Schiffelers & Yonas M. Tesfamariam & Lea-Marie Jenster & Stefan Diehl & Sophie C. Binder & Sabine Normann & Jonathan Mayr & Steffen Pritzl & Elena Hagelauer & Anja Kopp & Assaf Alon & Matth, 2024. "Antagonistic nanobodies implicate mechanism of GSDMD pore formation and potential therapeutic application," Nature Communications, Nature, vol. 15(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:nature:v:467:y:2010:i:7312:d:10.1038_nature09337. 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.