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

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.

Pubmed ID: 9950424


  • Kong YY
  • Yoshida H
  • Sarosi I
  • Tan HL
  • Timms E
  • Capparelli C
  • Morony S
  • Oliveira-dos-Santos AJ
  • Van G
  • Itie A
  • Khoo W
  • Wakeham A
  • Dunstan CR
  • Lacey DL
  • Mak TW
  • Boyle WJ
  • Penninger JM



Publication Data

January 28, 1999

Associated Grants


Mesh Terms

  • Animals
  • B-Lymphocytes
  • Bone Remodeling
  • Carrier Proteins
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines
  • Dendritic Cells
  • Embryonic and Fetal Development
  • Female
  • Gene Targeting
  • Growth Substances
  • Hematopoiesis, Extramedullary
  • Hematopoietic Stem Cells
  • Leukopoiesis
  • Lymph Nodes
  • Lymphocyte Activation
  • Lymphocytes
  • Male
  • Membrane Glycoproteins
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Molecular Sequence Data
  • Mutagenesis
  • Osteoclasts
  • Osteogenesis
  • Osteopetrosis
  • RANK Ligand
  • Receptor Activator of Nuclear Factor-kappa B
  • T-Lymphocytes
  • Thymus Gland