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Objectives To explore the pathogenesis of rheumatoid arthritis (RA) by studying the expression of T cell receptors (TCRs).Methods T cell receptor Vβ (TCR Vβ) gene usage and expression were analyzed from synovial membrane and peripheral blood of 8 RA patients, 2 osteoarthritis patients and 2 accident amputees. The complementary determining region 3 (CDR3) of 25 TCR Vβ subfamily genes in unselected T cell populations were amplified semi-quantitatively by reverse transcription-polymerase chain reaction (RT-PCR). The products were further studied by genescan for frequency of Vβ usage.Results The numbers of Vβ subfamilies expressed by T cells from RA peripheral blood and synovial membrane were not significantly restricted. More importantly, biased Vβ gene expression in RA synovium was observed and Vβ6, Vβ17, and Vβ22 genes were the predominant subfamilies. It was noteworthy that the expression of Vβ17 in RA synovium was significantly increased. Conclusion Our data were consistent with the hypothesis that several antigen or superantigen-driven processes may be involved in the pathogenesis of RA.
Objectives To explore the pathogenesis of rheumatoid arthritis (RA) by studying the expression of T cell receptors (TCRs). Methods T cell receptor Vβ (TCR Vβ) gene usage and expression were analyzed from synovial membrane and peripheral blood of 8 RA patients, 2 The products were further studied by RT-PCR. The products of the TCR Vβ subfamily genes in unselected T cell populations were amplified semi-quantitatively by reverse transcription-polymerase chain reaction (RT-PCR). genescan for frequency of Vβ usage. Results of The numbers of Vβ subfamilies expressed by T cells from RA peripheral blood and synovial membrane were not significantly restricted. More importantly, biased Vβ gene expression in RA synovium was observed and Vβ6, Vβ17, and Vβ22 genes were the was predominant subfamilies. It was noteworthy that the expression of Vβ17 in RA synovium was significantly increased. Conclusion Our data were con sistent with the hypothesis that several antigen or superantigen-driven processes may be involved in the pathogenesis of RA.