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This article is part of the supplement: 25th European Workshop for Rheumatology Research

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Altered composition of CD97 splice variants in rheumatoid synovial tissue

FA van Gaalen1, TCTM van der Pouw Kraan2, RGHH Nelissen3, TWJ Huizinga1 and CL Verweij2

Author affiliations

1 Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands

2 Department of Molecular Cell Biology, Free University Medical Center, Amsterdam, The Netherlands

3 Department of Orthopedic Surgery, Leiden University Medical Center, Leiden, The Netherlands

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Citation and License

Arthritis Research & Therapy 2005, 7(Suppl 1):P16  doi:10.1186/ar1537

The electronic version of this article is the complete one and can be found online at:

Received:11 January 2005
Published:17 February 2005

© 2005 BioMed Central Ltd

Poster presentation

The intimal lining of synovial tissue consists of fibroblast-like synoviocytes (type A synoviocytes) and macrophages (type B synoviocytes). These cells are able to interact through the CD97/CD55 receptor ligand system. The CD97 receptor is a heterodimer receptor composed of an alpha and a beta subunit. The CD97alpha subunit may exist as three isoforms due to alternative spliced transcripts, each having a different affinity for CD55.

When comparing synovium of rheumatoid arthritis (RA) patients with synovium of patients with osteoarthritis (OA), no increase in the level of total of CD97alpha or in the level of CD97beta transcripts was found. However, in RA synovium a relative increased expression of CD97 transcripts encoding isoforms with an increased affinity for CD55 (CD97alpha2 and CD97alpha3 mRNA) was detected. A difference in CD97 splice variants between RA and OA tissues could not be attributed to differences in composition of cells as in both tissues the majority of CD97+ cells were CD14+ macrophages/monocytes – 93% in RA and 94% in OA, respectively.

These data indicate that during inflammation CD97 splicing is regulated, and we propose that this is likely to affect trafficking and functioning of CD97-positive leukocytes.