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The HIV co-receptor CCR5 regulates osteoclast function

Ji-Won Lee1, Akiyoshi Hoshino2, Kazuki Inoue3

  • 1Division of Bio-Imaging, Proteo-Science Center (PROS), Ehime University, Ehime, 791-0295, Japan. jwlee@m.ehime-u.ac.jp.

Nature Communications
|December 22, 2017
PubMed

Insights

C-C chemokine receptor 5 (CCR5) regulates osteoclast function, impacting bone destruction. Blocking CCR5 impairs osteoclast activity, offering potential therapeutic targets for bone diseases.

Area of Science:

  • Immunology
  • Bone Biology
  • Cell Biology

Background:

  • C-C chemokine receptor 5 (CCR5) is a known co-receptor for HIV entry.
  • CCR5's absence correlates with reduced HIV transmission and bone-destructive diseases.
  • Its role in bone cell regulation remains largely uncharacterized.

Purpose of the Study:

  • To investigate the role of CCR5 in osteoclast function and bone metabolism.
  • To determine if CCR5 blockade affects osteoclast activity and bone resorption.

Main Methods:

  • In vitro studies using human osteoclasts and specific CCR5-blocking antibodies.
  • In vivo studies utilizing Ccr5-deficient (Ccr5-/-) mice.
  • Assessment of osteoclast function, cellular locomotion, and bone resorption activity.

Main Results:

  • CCR5 blockade in vitro significantly impaired human osteoclast function.
  • Ccr5-/- mice exhibited dysfunctional osteoclasts and resistance to RANKL-induced osteoporosis.
  • CCR5 deficiency led to impaired osteoclast locomotion and bone resorption, linked to podosome and Pyk2 disarrangement.

Conclusions:

  • CCR5 plays a critical role in regulating osteoclast function.
  • CCR5 is essential for bone resorption and is implicated in bone-destructive conditions.
  • Targeting CCR5 presents a potential therapeutic strategy for osteoporosis and other bone diseases.

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