IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v456y2008i7224d10.1038_nature07468.html
   My bibliography  Save this article

Structural recognition and functional activation of FcγR by innate pentraxins

Author

Listed:
  • Jinghua Lu

    (Structural Immunology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA)

  • Lorraine L. Marnell

    (University of New Mexico, Albuquerque, New Mexico 87131, USA)

  • Kristopher D. Marjon

    (University of New Mexico, Albuquerque, New Mexico 87131, USA)

  • Carolyn Mold

    (University of New Mexico, Albuquerque, New Mexico 87131, USA)

  • Terry W. Du Clos

    (University of New Mexico, Albuquerque, New Mexico 87131, USA
    VA Medical Center, Albuquerque, New Mexico 87108, USA)

  • Peter D. Sun

    (Structural Immunology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA)

Abstract

Pentraxins involved in FcγR activation The classical pentraxins, serum amyloid P component (SAP) and C-reactive protein (CRP), are major acute phase reactants in mouse and man. As shown in this paper, pentraxins recognize various FcγRs, and SAP opsonization activates FcγR-mediated phagocytosis and cytokine secretion. The receptor binding sites for SAP and IgG overlap resulting in competition of IgG binding to FcγR as well as inhibition of immune complex-mediated phagocytosis by soluble pentraxins.

Suggested Citation

  • Jinghua Lu & Lorraine L. Marnell & Kristopher D. Marjon & Carolyn Mold & Terry W. Du Clos & Peter D. Sun, 2008. "Structural recognition and functional activation of FcγR by innate pentraxins," Nature, Nature, vol. 456(7224), pages 989-992, December.
  • Handle: RePEc:nat:nature:v:456:y:2008:i:7224:d:10.1038_nature07468
    DOI: 10.1038/nature07468
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature07468
    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/nature07468?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.

    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:456:y:2008:i:7224:d:10.1038_nature07468. 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.