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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Cyclodextrin Inhibits Caveolin-1 to Regulate CD4+ T Cell Subset Differentiation and Ameliorate Rheumatoid Arthritis
Yajie Gao1, Peiyao Zhang2, Yinping Huo1,3
1The Central Lab, The First Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, China, btmc.cn.
Journal of Immunology Research
|August 13, 2026
Summary
Caveolin-1 (CAV-1) is elevated in rheumatoid arthritis (RA) and drives disease by altering CD4+ T cell differentiation. Inhibiting CAV-1 may offer a new therapeutic approach for RA patients.
Area of Science:
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is an autoimmune disease involving T cell-mediated inflammation.
- Caveolin-1 (CAV-1) is involved in immune cell signaling, but its role in RA is unknown.
Purpose of the Study:
- To investigate CAV-1 expression and its clinical relevance in RA.
- To determine CAV-1's role in CD4+ T cell dysfunction in RA pathogenesis.
Main Methods:
- Serum, CD4+ T cells, and synovial tissue from RA patients and controls were analyzed for CAV-1.
- A collagen-induced arthritis (CIA) mouse model was treated with a CAV-1 inhibitor (HP-β-CD).
- Joint pathology, T cell infiltration, differentiation, and cytokine levels were assessed.
Main Results:
- CAV-1 levels were higher in RA patients and correlated with disease markers (Anti-CCP, RF).
- HP-β-CD treatment reduced joint damage and inflammation in CIA mice.
- CAV-1 inhibition suppressed CD4+ T cell infiltration and differentiation (Th1, Th17, Treg), lowering pro-inflammatory cytokines.
Conclusions:
- Aberrant CAV-1 upregulation contributes to RA pathogenesis via CD4+ T cell regulation.
- Targeting CAV-1 presents a potential diagnostic and therapeutic strategy for RA.
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