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Annals of the Rheumatic Diseases 1997;56:613-620; doi:10.1136/ard.56.10.613
Copyright © 1997 BMJ Publishing Group Ltd & European League Against Rheumatism.
Ann Rheum Dis 1997;56:613-620 ( October )

Extended reports

Long term persistent accumulation of CD8+ T cells in synovial fluid of rheumatoid arthritis Kayo Masuko-Hongo,a Taichi Sekine,a Shinichiro Ueda,a Tetsuji Kobata,a Kazuhiko Yamamoto,b Kusuki Nishioka,a Tomohiro Katoa

a Rheumatology, Immunology and Genetics Programme, Institute of Medical Science, St Marianna University, Kawasaki, Japan , b Medical Institute of Bioregulation, Kyushu University, Oita, Japan

Correspondence to: Dr K Masuko-Hongo, Rheumatology, Immunology and Genetics Programme, Institute of Medical Science, St Marianna University, 2-16-1 Sugao, Miyamae-ku, Kawasaki, Kanagawa 216, Japan.

Accepted for publication 21 July 1997

OBJECTIVE---To characterise the type and kinetics of T cell clones in synovial lesions of patients with rheumatoid arthritis (RA).
METHODS---Mononuclear cells from serial samples of synovial fluid (SF) and peripheral blood from nine RA patients were separated phenotypically using antibody coated magnetic beads. After mRNA preparation, reverse transcription-polymerase chain reaction (RT-PCR) was performed to amplify V-D(N)-J (that is, the third complementarity determining, CDR3) regions of their T cell receptor beta chain genes. This was followed by single strand conformation polymorphism (SSCP) analysis to detect the clonotypes of accumulating T cells. Amino acid sequences of the dominant clones were also determined.
RESULTS---Although peripheral T cells were heterogeneous, accumulation of oligoclonal T cells was detected in SF. The predominant accumulating clone was the CD8 subset, which was persistently present in serial samples obtained over almost one year of follow up. A proportion of these cells expressed CD25 or CD45RO, or both, suggesting they are `memory' clones.
CONCLUSION---The persistent presence of CD8+ T cell clones in RA joints indicates that they may be involved in the perpetuation of the chronic inflammatory process in RA joints.


© 1997 by Annals of the Rheumatic Diseases

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