IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v397y1999i6717d10.1038_16852.html
   My bibliography  Save this article

OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis

Author

Listed:
  • Young-Yun Kong

    (Ontario Cancer Institute, University of Toronto)

  • Hiroki Yoshida

    (Ontario Cancer Institute, University of Toronto)

  • Ildiko Sarosi

    (Amgen Inc., One Amgen Center Drive)

  • Hong-Lin Tan

    (Amgen Inc., One Amgen Center Drive)

  • Emma Timms

    (Amgen Inc., One Amgen Center Drive)

  • Casey Capparelli

    (Amgen Inc., One Amgen Center Drive)

  • Sean Morony

    (Amgen Inc., One Amgen Center Drive)

  • Antonio J. Oliveira-dos-Santos

    (Ontario Cancer Institute, University of Toronto)

  • Gwyneth Van

    (Amgen Inc., One Amgen Center Drive)

  • Annick Itie

    (Ontario Cancer Institute, University of Toronto)

  • Wilson Khoo

    (Ontario Cancer Institute, University of Toronto)

  • Andrew Wakeham

    (Ontario Cancer Institute, University of Toronto)

  • Colin R. Dunstan

    (Amgen Inc., One Amgen Center Drive)

  • David L. Lacey

    (Amgen Inc., One Amgen Center Drive)

  • Tak W. Mak

    (Ontario Cancer Institute, University of Toronto)

  • William J. Boyle

    (Amgen Inc., One Amgen Center Drive)

  • Josef M. Penninger

    (Ontario Cancer Institute, University of Toronto)

Abstract

The tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and ODF) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph-node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.

Suggested Citation

  • Young-Yun Kong & Hiroki Yoshida & Ildiko Sarosi & Hong-Lin Tan & Emma Timms & Casey Capparelli & Sean Morony & Antonio J. Oliveira-dos-Santos & Gwyneth Van & Annick Itie & Wilson Khoo & Andrew Wakeham, 1999. "OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis," Nature, Nature, vol. 397(6717), pages 315-323, January.
  • Handle: RePEc:nat:nature:v:397:y:1999:i:6717:d:10.1038_16852
    DOI: 10.1038/16852
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/16852
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/16852?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. Tang-Chuan Wang & Che-Chen Lin & Chia-Der Lin & Hsiung-Kwang Chung & Ching-Yuang Wang & Ming-Hsui Tsai & Chia-Hung Kao, 2015. "Increased Acquired Cholesteatoma Risk in Patients with Osteoporosis: A Retrospective Cohort Study," PLOS ONE, Public Library of Science, vol. 10(7), pages 1-10, July.
    2. Yongkuk Park & Tadatoshi Sato & Jungwoo Lee, 2023. "Functional and analytical recapitulation of osteoclast biology on demineralized bone paper," Nature Communications, Nature, vol. 14(1), pages 1-16, 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:397:y:1999:i:6717:d:10.1038_16852. 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.