Publication

The Role of IL-17 and TH17 Cells in the Bone Catabolic Activity of PTH

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Last modified
  • 02/20/2025
Type of Material
Authors
    Roberto Pacifici, Emory University
Language
  • English
Date
  • 2016-02-17
Publisher
  • Frontiers Media
Publication Version
Copyright Statement
  • © 2016 Pacifici.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1664-3224
Volume
  • 7
Start Page
  • 57
End Page
  • 57
Grant/Funding Information
  • This paper was supported by grants from the National Institutes of Health (AR54625, DK007298, and RR028009).
Abstract
  • Osteoimmunology is field of research dedicated to the study of the interactions between the immune system and bone. Among the cells of the immune system that regulate the skeleton in health and disease are T lymphocytes, T cells secrete inflammatory/osteoclastogenic cytokines such as RANKL, TNF, and IL-17, as well as factors that stimulate bone formation, including Wnt ligands. In addition, T cells regulate the differentiation and life span of stromal cells via CD40L and other costimulatory molecules expressed on their surface. Consensus exists that parathyroid hormone (PTH) induces bone loss by increasing the production of RANKL by osteocytes and osteoblast. However, new evidence suggests that PTH expands Th17 cells and increases IL-17 levels in mice and humans. Studies in the mouse of further shown that Th17 cell produced IL-17 acts as an "upstream cytokine" that increases the sensitivity of osteoblasts and osteocytes to PTH. As a result, PTH stimulates osteocytic and osteoblastic release of RANKL. Therefore, PTH cause bone loss only in the presence of IL-17 signaling. This article reviews the evidence that the effects of PTH are mediated not only by osteoblasts and osteocytes, but also T cells and IL-17.
Author Notes
Keywords
Research Categories
  • Biology, Physiology
  • Health Sciences, Immunology

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