Discrepancy in T cell clonal expansions in synovial fluid and peripheral blood from rheumatoid arthritis patients.
- Author:
In Hong CHOI
1
;
Youngjoon CHWAE
;
Soo Kon LEE
;
Minkyung CHU
;
Joo Deuk KIM
;
Se Jong KIM
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: Rheumatoid arthritis; synovial fluid T cells; T cell receptor; CDR3; clonal expansions; DR+ T cells
- MeSH: Arthritis, Rheumatoid/*metabolism/pathology; Base Sequence; Blood Cells/*metabolism; Clone Cells; Female; Human; Male; Molecular Probes; Molecular Sequence Data; Polymerase Chain Reaction; Receptors, Antigen, T-Cell/genetics/*metabolism; Support, Non-U.S. Gov't; Synovial Fluid/cytology/*metabolism; T-Lymphocytes/*metabolism
- From:Yonsei Medical Journal 1995;36(1):68-76
- CountryRepublic of Korea
- Language:English
- Abstract: Rheumatoid arthritis (RA) is an autoimmune disease involving the synovial membrane of peripheral joints. T cells specific for self antigens may play a critical role. Identification of T cell receptors (TCR) of such specific T cell clones is very important for treatment, prevention and identification of relevant autoantigens. To identify specific T cells, TCR V beta family repertoire and the clonal expansion of T cells were analyzed in this study. The percentage of V beta 5+ or V beta 8+ cells in the synovial fluid mononuclear cells (SFMCs) was similar to that in the peripheral blood mononuclear cells (PBMCs). However, the percentage of DR+ T cells in the SFMCs was higher (p< 0.01). Analyzing the clonality of T cells in 8 V beta families (V beta 1, V beta 5, V beta 8, V beta 14, V beta 16, V beta 17, V beta 18, V beta 20), clonal expansions in CD8+ T cells from the SFMCs were found more frequently than in the PBMCs. The patterns of clonal expansions were discrepant between the SFMCs and the PBMCs even in the same patient, which suggests several inflamed tissue specific T cell clonal expansions in the SFMCs. These T cell clones might be activated by autoantigens which are not identified yet and responsible for the RA pathogenesis.
