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Related Experiment Videos

Parathyroid Diseases and T Cells.

M Neale Weitzmann1,2,3, Roberto Pacifici4,5

  • 1Atlanta U.S. Department of Veterans Affairs Medical Center, Decatur, GA, 30033, USA. mweitzm@emory.edu.

Current Osteoporosis Reports
|April 20, 2017
PubMed
Summary

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T cells play a permissive role in hyperparathyroidism-induced bone loss by amplifying bone resorption. These immune cells promote pathways that increase the RANKL/OPG ratio, contributing to bone catabolism.

Area of Science:

  • Immunology
  • Endocrinology
  • Bone Biology

Background:

  • Hyperparathyroidism and parathyroid hormone (PTH) contribute to bone loss.
  • The role of T cells in this process is increasingly recognized.

Purpose of the Study:

  • To review the permissive role of T cells in PTH-induced bone catabolism.
  • To elucidate the mechanisms by which T cells amplify bone resorption.

Main Methods:

  • Review of animal studies and translational human studies.
  • Analysis of molecular pathways involving T cell subsets (CD4+, Th17) and cytokines (TNFα, IL-17A).

Main Results:

  • T cells potently amplify PTH-induced bone resorption.
  • PTH exploits CD4+ T cells to increase TNFα production, promoting Th17 cell differentiation.
Keywords:
HyperparathyroidismOsteoimmunologyOsteoporosisPTHParathyroid hormoneT cells

Related Experiment Videos

  • TNFα and IL-17A amplify RANKL production and down-regulate OPG, favoring osteoclast activity.

    • Conclusions:

    • T cells significantly amplify traditional pathways of PTH-induced bone loss.
    • T cells provide costimulatory signals that favor an increased RANKL/OPG ratio, leading to bone resorption.