CD97 neutralisation increases resistance to collagen-induced arthritis in mice |
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Authors: | Else N Kop Janik Adriaansen Tom JM Smeets Margriet J Vervoordeldonk René AW van Lier Jörg Hamann Paul P Tak |
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Institution: | (1) Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Amsterdam, P.O. Box 22700, 1100, DE, Amsterdam, The Netherlands;(2) Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100, DE, Amsterdam, The Netherlands |
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Abstract: | Synovial tissue of rheumatoid arthritis (RA) patients is characterised by an influx and retention of CD97-positive inflammatory
cells. The ligands of CD97, CD55, chondroitin sulfate B, and α5β1 (very late antigen VLA]-5) are expressed abundantly in
the synovial tissue predominantly on fibroblast-like synoviocytes, endothelium, and extracellular matrix. Based upon this
expression pattern, we hypothesise CD97 expression to result in accumulation of inflammatory cells in the synovial tissue
of RA patients. To determine the therapeutic effect of blocking CD97 in an animal model of RA, collagen-induced arthritis
was induced in a total of 124 DBA/J1 mice. Treatment was started on day 21 (early disease) or on day 35 (longstanding disease)
with the blocking hamster anti-mouse CD97 monoclonal antibody (mAb) 1B2, control hamster immunoglobulin, or NaCl, applied
intraperitoneally three times a week. The paws were evaluated for clinical signs of arthritis and, in addition, examined by
radiological and histological analysis. Mice receiving 0.5 mg CD97 mAb starting from day 21 had significantly less arthritis
activity and hind paw swelling. Furthermore, joint damage and inflammation were reduced and granulocyte infiltration was decreased.
When treatment was started on day 35, CD97 mAb treatment had similar effects, albeit less pronounced. The results support
the notion that CD97 contributes to synovial inflammation and joint destruction in arthritis. |
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