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Peer-reviewedCC BY 4.0Journal of Immunology Research

Research Advances in Targeted Modulation of Macrophage M1/M2 Polarization for the Treatment of Rheumatoid Arthritis

  • Hui Zuo1,2
  • Enqi Fan1
  • Long Zeng1
  • Jun Hu1
  • Jiajia Sang2
  • Feng Hao1
  1. 1Nanjing University of Chinese Medicine Nanjing 210023 China njucm.edu.cn
  2. 2The Affiliated Hospital of Nanjing University of Chinese Medicine Nanjing 210029 China njucm.edu.cn
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Abstract

Rheumatoid arthritis (RA) is a disease of the immune system that leads to continuous synovial inflammation and the progressive breakdown of joints. As essential effector cells in innate immunity, macrophages can become either pro‐inflammatory M1 or anti‐inflammatory M2 phenotypes, playing a critical role in RA pathogenesis. A marked M1/M2 polarization imbalance exists in the synovial microenvironment of RA, in which excessive activation and accumulation of M1 macrophages serve as a key hub driving persistent inflammation, cartilage degradation, and bone erosion. Currently, conventional disease‐modifying antirheumatic drugs (DMARDs) with methotrexate (MTX) as the anchor agent remain the mainstay for RA management; however, approximately 30%‐40% of RA patients show an inadequate response to MTX, resulting in persistent synovial inflammation, progressive joint damage, and difficult‐to‐control disease. For macrophage‐directed phenotypic modulation in RA therapy, novel smart nanodelivery systems are a key research focus, while accumulating preclinical evidence supports the capacity of traditional Chinese medicine (TCM) to restore M1/M2 homeostasis. This review systematically summarizes the polarization mechanisms of macrophages in RA, their core pathological functions, and recent advances in targeting these cells as therapeutic strategies, therefore delivering novel insights and references for RA treatment through targeted changes in macrophage polarization.

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Cite

BibTeXRIS
BibTeX
@article{zuo2026research,
  title = {{Research Advances in Targeted Modulation of Macrophage M1/M2 Polarization for the Treatment of Rheumatoid Arthritis}},
  author = {Hui Zuo and Enqi Fan and Long Zeng and Jun Hu and Jiajia Sang and Feng Hao},
  journal = {Journal of Immunology Research},
  year = {2026},
  month = nov,
  doi = {10.1155/jimr/4203230},
  url = {https://doi.org/10.1155/jimr/4203230},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Research Advances in Targeted Modulation of Macrophage M1/M2 Polarization for the Treatment of Rheumatoid Arthritis
AU  - Hui Zuo
AU  - Enqi Fan
AU  - Long Zeng
AU  - Jun Hu
AU  - Jiajia Sang
AU  - Feng Hao
PY  - 2026
DA  - 2026/11/02
JO  - Journal of Immunology Research
DO  - 10.1155/jimr/4203230
UR  - https://doi.org/10.1155/jimr/4203230
AB  - Rheumatoid arthritis (RA) is a disease of the immune system that leads to continuous synovial inflammation and the progressive breakdown of joints. As essential effector cells in innate immunity, macrophages can become either pro‐inflammatory M1 or anti‐inflammatory M2 phenotypes, playing a critical role in RA pathogenesis. A marked M1/M2 polarization imbalance exists in the synovial microenvironment of RA, in which excessive activation and accumulation of M1 macrophages serve as a key hub driving persistent inflammation, cartilage degradation, and bone erosion. Currently, conventional disease‐modifying antirheumatic drugs (DMARDs) with methotrexate (MTX) as the anchor agent remain the mainstay for RA management; however, approximately 30%‐40% of RA patients show an inadequate response to MTX, resulting in persistent synovial inflammation, progressive joint damage, and difficult‐to‐control disease. For macrophage‐directed phenotypic modulation in RA therapy, novel smart nanodelivery systems are a key research focus, while accumulating preclinical evidence supports the capacity of traditional Chinese medicine (TCM) to restore M1/M2 homeostasis. This review systematically summarizes the polarization mechanisms of macrophages in RA, their core pathological functions, and recent advances in targeting these cells as therapeutic strategies, therefore delivering novel insights and references for RA treatment through targeted changes in macrophage polarization.
SN  - 2314-8861
SN  - 2314-7156
ER  -