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Updated: Jun 4, 2026
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Essential role of microRNA-155 in the pathogenesis of autoimmune arthritis in mice
Stephan Blüml1, Michael Bonelli, Birgit Niederreiter
1Medical University of Vienna, Vienna, Austria.
Objective:
MicroRNAs (miRNA) are a new class of regulatory elements. Altered expression of miRNA has been demonstrated in the inflamed joints of patients with rheumatoid arthritis (RA). The aim of this study was to examine the role of miRNA in the pathogenesis of autoimmune arthritis, using 2 murine models.
Methods:
Collagen-induced arthritis (CIA) and K/BxN serum-transfer arthritis were induced in wild-type (WT) and miR-155-deficient (miR-155(-/-) ) mice. The severity of arthritis was determined clinically and histologically. Anticollagen antibodies and cytokines were measured by enzyme-linked immunosorbent assay. The cellular composition of the draining lymph nodes after induction of CIA was measured by flow cytometry.
Results:
The miR-155(-/-) mice did not develop CIA. Deficiency in miR-155 prevented the generation of pathogenic autoreactive B and T cells, since anticollagen antibodies and the expression levels of antigen-specific T cells were strongly reduced in miR-155(-/-) mice. Moreover, Th17 polarization of miR-155(-/-) mouse T cells was impaired, as shown by a significant decrease in the levels of interleukin-17 (IL-17) and IL-22. In the K/BxN serum-transfer arthritis model, which only depends on innate effector mechanisms, miR-155(-/-) mice showed significantly reduced local bone destruction, attributed to reduced generation of osteoclasts, although the severity of joint inflammation was similar to that in WT mice.
Conclusion:
These results demonstrate that miR-155 is essentially involved in the adaptive and innate immune reactions leading to autoimmune arthritis, and therefore miR-155 might provide a novel target for the treatment of patients with RA.
Insights
MicroRNA-155 (miR-155) plays a crucial role in autoimmune arthritis development. Its deficiency prevents pathogenic immune cell generation and reduces bone destruction in mouse models, suggesting miR-155 as a potential therapeutic target for rheumatoid arthritis.
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- MicroRNAs (miRNAs) are key regulatory elements in cellular processes.
- Dysregulated miRNA expression is observed in rheumatoid arthritis (RA) joint inflammation.
- The specific role of miRNAs in autoimmune arthritis pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the role of microRNA-155 (miR-155) in the pathogenesis of autoimmune arthritis.
- To utilize two distinct murine models of arthritis to elucidate miR-155's function.
- To assess the impact of miR-155 deficiency on adaptive and innate immune responses in arthritis.
Main Methods:
- Induction of collagen-induced arthritis (CIA) and K/BxN serum-transfer arthritis in wild-type and miR-155-deficient mice.
- Clinical and histological assessment of arthritis severity.
- Measurement of anti-collagen antibodies, cytokines (IL-17, IL-22), and cellular composition via ELISA and flow cytometry.
Main Results:
- miR-155 deficiency completely prevented the development of CIA.
- Absence of miR-155 reduced pathogenic autoreactive B and T cell generation, including Th17 polarization.
- In the K/BxN model, miR-155 deficiency decreased osteoclast generation and subsequent bone destruction, while joint inflammation severity remained similar.
Conclusions:
- miR-155 is integral to both adaptive and innate immune responses driving autoimmune arthritis.
- Targeting miR-155 presents a potential novel therapeutic strategy for rheumatoid arthritis.
- These findings highlight miR-155's critical role in immune-mediated joint diseases.
