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Pathogenesis of polymyalgia rheumatica.

G Guggino1, A Ferrante, F Macaluso

  • 1Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo. giuliana.guggino@unipa.it.

Reumatismo
|March 29, 2018
PubMed
Summary
This summary is machine-generated.

Polymyalgia rheumatica (PMR) is an inflammatory disease primarily affecting those over 50. Recent findings reveal complex immune system involvement, including dendritic cells, macrophages, and altered T cell balance, contributing to PMR pathogenesis.

Keywords:
Adaptive immunityInnate immunityPathogenesis.Polymyalgia rheumatica

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Area of Science:

  • Rheumatology
  • Immunology
  • Geriatric Medicine

Background:

  • Polymyalgia rheumatica (PMR) is a chronic inflammatory condition predominantly affecting individuals over 50.
  • Its exact cause remains unknown, though age-related immune changes and genetic predisposition are suspected.
  • PMR is frequently associated with giant cell arteritis.

Purpose of the Study:

  • To review recent advancements in understanding the pathogenesis of Polymyalgia Rheumatica.
  • To explore the roles of immune system activation and cellular alterations in PMR development.

Main Methods:

  • Review of current scientific literature on PMR pathogenesis.
  • Analysis of studies investigating immune cell activation and function in PMR patients.

Main Results:

  • Evidence confirms activation of innate and adaptive immune systems in PMR.
  • Key findings include activated dendritic cells and monocytes/macrophages.
  • An altered balance between T helper 17 (Th17) and regulatory T (Treg) cells is observed.
  • Disturbances in B cell distribution and function are also noted.

Conclusions:

  • PMR pathogenesis is more complex than previously understood.
  • Age-related immune alterations likely play a significant role in genetically susceptible individuals.
  • Immune system dysregulation involving multiple cell types is central to PMR development.