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Updated: Dec 23, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Self-reactive T cells induce and perpetuate chronic relapsing arthritis
Jonatan Tuncel1, Jens Holmberg2, Sabrina Haag1
1Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
CD4+ T cells from lymph nodes drive chronic relapsing arthritis in rats, while spleen T cells cause acute disease. Interleukin-17 (IL-17) is crucial for sustaining this T cell-mediated inflammation.
Area of Science:
- Immunology
- Rheumatology
- Autoimmunity
Background:
- CD4+ T cells are key in early rheumatoid arthritis (RA).
- Their role in sustaining chronic, relapsing RA remains unclear.
- Understanding T cell contribution is vital for RA pathogenesis.
Purpose of the Study:
- To provide conclusive evidence that T cells drive chronic relapsing arthritis.
- To investigate the mechanisms of T cell-mediated chronic inflammation in RA.
Main Methods:
- Utilized the rat pristane-induced arthritis (PIA) model.
- Administered CD4+ T cells from lymph nodes versus spleen into irradiated rats.
- Investigated the impact of thymectomy and T cell depletion.
Main Results:
- Lymph node-derived CD4+ T cells induced chronic arthritis (>4 months); spleen cells induced acute disease.
- Thymectomy enhanced arthritis severity, suggesting lymphopenia promotes T cell-driven inflammation.
- Chronic arthritis correlated with Th17 transcripts; IL-17 neutralization led to sustained remission.
Conclusions:
- Activated self-reactive T cells can sustain inflammation long-term.
- Interleukin-17 (IL-17) plays a critical role in promoting sustained T cell-driven inflammation.
- Targeting IL-17 may be a viable strategy for managing chronic RA.
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