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Chronic Inflammation: Introduction01:12

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Related Experiment Video

Updated: May 22, 2026

Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue
09:18

Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue

Published on: February 24, 2023

Macrophages in synovial inflammation.

Aisling Kennedy1, Ursula Fearon, Douglas J Veale

  • 1School of Medicine and Medical Sciences, University College Dublin Conway Institute Dublin, Ireland.

Frontiers in Immunology
|May 9, 2012
PubMed
Summary

Synovial macrophages in rheumatoid arthritis (RA) joints become activated, driving inflammation and joint destruction. Targeting macrophage polarization offers a potential new therapeutic strategy for RA.

Keywords:
arthritisinflammationmacrophage

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Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • Synovial macrophages are key cells in healthy and inflamed joints.
  • Activated macrophages contribute to inflammation and joint destruction in rheumatoid arthritis (RA).
  • Sub-lining macrophages are a reliable biomarker for RA disease severity and treatment response.

Purpose of the Study:

  • To review the current understanding of macrophage polarization in RA.
  • To explore molecular drivers controlling macrophage polarization.
  • To discuss novel therapeutic paradigms targeting macrophage phenotype.

Main Methods:

  • Review of existing literature on synovial macrophages, inflammation, and RA.
  • Analysis of molecular mechanisms regulating macrophage polarization (cytokines, transcription factors, lipid mediators).

Main Results:

  • Inflammatory synovial macrophages are implicated in RA pathogenesis.
  • M1 macrophage-associated cytokines (TNFα, IL-1) are abundant in RA, while M2 markers (IL-10) are diminished.
  • Pro-resolving lipid mediators may promote a non-inflammatory macrophage phenotype.

Conclusions:

  • Macrophage phenotype critically influences RA.
  • Understanding macrophage polarization is crucial for developing new RA therapies.
  • Targeting macrophage polarization pathways presents a novel therapeutic avenue for RA.