Expression of the activation antigen CD97 and its ligand CD55 in rheumatoid synovial tissue
Open Access
- 1 April 1999
- journal article
- basic science
- Published by Wiley in Arthritis & Rheumatism
- Vol. 42 (4) , 650-658
- https://doi.org/10.1002/1529-0131(199904)42:4<650::aid-anr7>3.0.co;2-s
Abstract
Objective Fibroblast‐like synoviocytes (FLS) express decay‐accelerating factor (CD55) at high levels. Recently, it was found that CD55 is a specific cellular ligand for the 7‐span transmembrane receptor CD97. The objective of this study was to define the expression of this receptor–ligand pair in synovial tissue (ST) to provide more insight into the interaction between FLS and surrounding cells. Methods Antibodies against CD97 and CD55 were used for immunohistologic analysis of synovial biopsy specimens from 16 patients with rheumatoid arthritis (RA) and 15 patients with osteoarthritis (OA). In addition, an enzyme‐linked immunosorbent assay system was used to determine the expression of soluble CD97 (sCD97) in synovial fluid (SF) from 30 patients with RA, 13 with OA, and 10 with reactive arthritis (ReA). Results In both RA and OA ST sections, strong expression of CD55 was confirmed on FLS in the intimal lining layer, where it was also found that all macrophages expressed CD97. The percentage of macrophages that expressed CD97 was lower in the synovial sublining (P = 0.005). The mean levels of sCD97 in SF were significantly higher in RA patients than in patients with OA or ReA (P < 0.0001). Conclusion These results suggest that FLS are able to interact with macrophages via the CD97/CD55 receptor–ligand system. In this respect, the CD97/CD55 pair may account for the specific architecture of the intimal lining layer and may be of primary importance in maintaining and amplifying synovial inflammation. The specific increase in sCD97 levels in RA SF might be related to the presence of activated proteolytic systems or to the increase in synovial mass, rather than a consequence of local receptor–ligand interaction.Keywords
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