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Updated: Nov 4, 2025
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
MicroRNA-26b-5p alleviates murine collagen-induced arthritis by modulating Th17 cell plasticity
Ming-Fei Zhang1, Pei Yang1, Mei-Yu Shen1
1School of Pharmacy, Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Nanjing University of Chinese Medicine, NO.138 Xianlin Road, 210023 Nanjing, Jiangsu Province, PR China.
Abstract:
Rheumatoid arthritis (RA) is a chronic autoimmune disease, and the abnormal differentiation of IL-17-producing T helper (Th17) cells is an important factor in the pathogenesis. Previous studies have shown that microRNAs (miRNAs, miR) act as key regulators of Th17 cells. However, the effects of miRNAs on Th17 cell differentiation and plasticity in RA are not clear. In this study, not only low miR-26b-5p expression and high IL-17A level were observed in the peripheral blood of RA patients, but also the negative correlation between miR-26b-5p and IL-17A was explored. The changes in collagen-induced arthritis (CIA) mice were consistent with those in RA patients. The results of in vitro experiments showed that miR-26b-5p mainly inhibited the initial differentiation of Th17 cells but did not impact the differentiation of induced-Treg into Th17-like cells. Meanwhile, miR-26b-5p mimics treatment alleviated inflammatory responses and reduced Th17 proportion in CIA mice. These results indicated that miR-26b-5p could alleviate the development of mice CIA by inhibiting the excessive Th17 cells, and that miR-26b-5p could modulate the plasticity of Th17 cell differentiation in RA, mainly block the initial differentiation. This may provide a novel strategy for the clinical treatment of RA.
Insights
MicroRNA-26b-5p (miR-26b-5p) inhibits T helper 17 (Th17) cell differentiation in rheumatoid arthritis (RA). This finding suggests miR-26b-5p as a potential therapeutic target for RA treatment.
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease driven by T helper 17 (Th17) cells.
- MicroRNAs (miRNAs) are known regulators of Th17 cell differentiation, but their specific roles in RA remain unclear.
Purpose of the Study:
- To investigate the role of miR-26b-5p in Th17 cell differentiation and plasticity in rheumatoid arthritis.
- To explore miR-26b-5p as a potential therapeutic target for RA.
Main Methods:
- Analysis of miR-26b-5p and IL-17A levels in RA patients' peripheral blood.
- Collagen-induced arthritis (CIA) mouse model to study Th17 cell differentiation in vivo.
- In vitro experiments to assess the effect of miR-26b-5p on Th17 cell differentiation and Treg plasticity.
Main Results:
- Lower miR-26b-5p and higher IL-17A levels were observed in RA patients, with a negative correlation between them.
- miR-26b-5p primarily inhibited the initial differentiation of Th17 cells, not induced-Treg to Th17-like cell conversion.
- miR-26b-5p treatment reduced inflammation and Th17 cell proportion in CIA mice.
Conclusions:
- miR-26b-5p alleviates CIA development in mice by suppressing excessive Th17 cell differentiation.
- miR-26b-5p modulates Th17 cell plasticity in RA, mainly by blocking initial differentiation.
- miR-26b-5p represents a potential novel therapeutic strategy for rheumatoid arthritis.
