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Updated: Jul 4, 2026
Murine Model of Epicutaneously-Induced Immunomodulation
Published on: June 24, 2025
Targeting the chemotactic function of CD147 reduces collagen-induced arthritis
Jesse M Damsker1, Ifeanyi Okwumabua, Tatiana Pushkarsky
1Department of Microbiology, Immunology and Tropical Medicine, The George Washington University, Washington, DC 20037, USA.
Insights
Blocking CD147-cyclophilin interactions with an antibody significantly reduced joint inflammation in a mouse model of rheumatoid arthritis (RA). This suggests CD147 plays a key role in recruiting inflammatory cells to joints in RA.
Area of Science:
- Immunology
- Cell Biology
- Rheumatology
Background:
- CD147 is a glycoprotein on leucocytes involved in cell migration.
- CD147 interacts with extracellular cyclophilins, potentially influencing inflammatory diseases like rheumatoid arthritis (RA).
- Increased CD147 and cyclophilin A are observed in RA patients' joints.
Purpose of the Study:
- To investigate the role of CD147-cyclophilin interactions in joint inflammation.
- To assess the therapeutic potential of targeting CD147 in collagen-induced arthritis.
Main Methods:
- Used a mouse model of collagen-induced arthritis.
- Treated leucocytes with anti-CD147 monoclonal antibody in vitro to assess migration.
- Administered anti-CD147 monoclonal antibody in vivo to evaluate arthritis development.
Main Results:
- Anti-CD147 antibody treatment inhibited leucocyte (neutrophils, monocytes, CD4+ T cells) migration in vitro.
- In vivo anti-CD147 antibody treatment reduced collagen-induced arthritis development by over 75%.
- CD147-cyclophilin interactions promote leucocyte recruitment to inflamed joints.
Conclusions:
- CD147-cyclophilin interactions are crucial for leucocyte recruitment in joint inflammation.
- Targeting CD147-cyclophilin interactions shows promise for treating rheumatoid arthritis.
- CD147 is a potential therapeutic target for inflammatory arthritis pathogenesis.
Abstract:
CD147 is a type I transmembrane glycoprotein expressed on a wide variety of cell types, including all leucocytes. While CD147 is best known as a potent inducer of matrix metalloproteinases, it can also function as a regulator of leucocyte migration through its cell surface interaction with chemotactic extracellular cyclophilins. A potential role for CD147-cyclophilin interactions during inflammatory diseases, including rheumatoid arthritis (RA), is suggested from several studies. For example, CD147 expression is increased on reactive leucocytes in the synovial fluid and tissues of patients with arthritis. In addition, the synovial fluid of patients with RA contains high levels of extracellular cyclophilin A. In the current studies we investigated the contribution of the chemotactic function of CD147-cyclophilin interactions to joint inflammation using the mouse model of collagen-induced arthritis. Our data demonstrate that proinflammatory leucocytes, specifically neutrophils, monocytes and activated CD4(+) T cells, lose their ability to migrate in response to cyclophilin A in vitro when treated with anti-CD147 monoclonal antibody. Furthermore, in vivo treatment with anti-CD147 monoclonal antibody can reduce the development of collagen-induced arthritis in mice by >75%. Such findings suggest that CD147-cyclophilin interactions might contribute to the pathogenesis of RA by promoting the recruitment of leucocytes into joint tissues.
