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Anti-IL-20 monoclonal antibody inhibits the differentiation of osteoclasts and protects against osteoporotic bone loss.

IL-20 is a proinflammatory cytokine of the IL-10 family that is involved in psoriasis, rheumatoid arthritis, atherosclerosis, and stroke. However, little is known about the role of IL-20 in bone destruction. We explored the function of IL-20 in osteoclastogenesis and the therapeutic potential of anti-IL-20 monoclonal antibody 7E for treating osteoporosis. Higher serum IL-20 levels were detected in patients with osteopenia and osteoporosis and in ovariectomized (OVX) mice. IL-20 mediates osteoclastogenesis by up-regulating the receptor activator of NF-κB (RANK) expression in osteoclast precursor cells and RANK ligand (RANKL) in osteoblasts. 7E treatment completely inhibited osteoclast differentiation induced by macrophage colony-stimulating factor (M-CSF) and RANKL in vitro and protected mice from OVX-induced bone loss in vivo. Furthermore, IL-20R1-deficient mice had significantly higher bone mineral density (BMD) than did wild-type controls. IL-20R1 deficiency also abolished IL-20-induced osteoclastogenesis and increased BMD in OVX mice. We have identified a pivotal role of IL-20 in osteoclast differentiation, and we conclude that anti-IL-20 monoclonal antibody is a potential therapeutic for protecting against osteoporotic bone loss.

Pubmed ID: 21844205

Authors

  • Hsu YH
  • Chen WY
  • Chan CH
  • Wu CH
  • Sun ZJ
  • Chang MS

Journal

The Journal of experimental medicine

Publication Data

August 29, 2011

Associated Grants

None

Mesh Terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Animals
  • Antibodies, Monoclonal, Murine-Derived
  • Antibodies, Neutralizing
  • Cell Differentiation
  • Female
  • Humans
  • Interleukins
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Middle Aged
  • Osteoclasts
  • Osteoporosis
  • Receptor Activator of Nuclear Factor-kappa B
  • Receptors, Interleukin
  • Up-Regulation