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Related Concept Videos

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T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Chronic Inflammation: Introduction

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Inflammatory Response

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Related Experiment Video

Updated: Jul 14, 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

Macrophage Metabolic Reprogramming in Rheumatoid Arthritis: Pathogenic Mechanisms and Therapeutic Implications.

Longping Chen1,2, Siyuan Leng3, Xin Liu2

  • 1School of Chinese Medical Sciences, Hunan University of Chinese Medicine, Changsha 410208, China.

Cells
|July 13, 2026
PubMed
Summary

Metabolic reprogramming in rheumatoid arthritis (RA) synovial macrophages sustains inflammation and tissue damage. Targeting macrophage metabolism offers potential therapeutic strategies for RA, but human validation is limited.

Keywords:
immunometabolismmacrophagesmetabolic reprogrammingrheumatoid arthritissynovial microenvironment

Related Experiment Videos

Last Updated: Jul 14, 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

Area of Science:

  • Immunology
  • Metabolism
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by synovitis, cartilage destruction, and bone erosion.
  • Synovial macrophages exhibit significant heterogeneity in RA, with metabolic reprogramming contributing to pathogenic functions.

Purpose of the Study:

  • To review the functional states and metabolic features of synovial macrophages in health and RA.
  • To explore how metabolic reprogramming in these cells drives inflammation, tissue remodelling, and bone destruction.
  • To assess the immunometabolic effects of current RA drugs and evaluate therapeutic strategies targeting macrophage metabolism.

Main Methods:

  • This is a narrative review synthesizing recent findings from single-cell/spatial omics and immunometabolic studies.
  • Focuses on the rewiring of glucose, lipid, and amino acid metabolism in synovial macrophages.
  • Appraises preclinical evidence and translational limitations of metabolic interventions.

Main Results:

  • Metabolic reprogramming sustains pathogenic macrophage states, intercellular communication, and inflammation resolution impairment in RA.
  • Connections between metabolism, inflammatory transcription, tissue remodelling, and bone destruction are mediated by metabolic enzymes, intermediates, redox, and epigenetics.
  • Current antirheumatic drugs have immunometabolic effects, but targeting macrophage metabolism faces translational limitations and requires further human validation.

Conclusions:

  • Metabolic reprogramming is a key driver of synovial macrophage heterogeneity and pathogenic functions in RA.
  • Therapeutic targeting of macrophage metabolism holds promise but requires more robust evidence from human studies.
  • Further research is needed to validate metabolic flux, cell-state specificity, and causal relationships in human synovium.