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Discrepancy in T cell clonal expansions in synovial fluid and peripheral blood from rheumatoid arthritis patients

Authors
 Choi In Hong  ;  Chwae Youngjoon  ;  Lee Soo Kon  ;  Chu Minkyung  ;  Kim Joo Deuk  ;  Kim Se Jong 
Citation
 YONSEI MEDICAL JOURNAL, Vol.36(1) : 68-76, 1995-03 
Journal Title
YONSEI MEDICAL JOURNAL
ISSN
 0513-5796 
Issue Date
1995-03
MeSH
Arthritis, Rheumatoid / metabolism* ; Arthritis, Rheumatoid / pathology ; Base Sequence ; Blood Cells / metabolism* ; Clone Cells ; Female ; Humans ; Male ; Molecular Probes ; Molecular Sequence Data ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell / genetics ; Receptors, Antigen, T-Cell / metabolism* ; Synovial Fluid / cytology ; Synovial Fluid / metabolism* ; T-Lymphocytes / metabolism*
Keywords
Rheumatoid arthritis ; synovial fluid T cells ; T cell receptor ; CDR3 ; clonal expansions ; DR+ T cells
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 β family repertoire and the clonal expansion of T cells were analyzed in this study. The percentage of V β 5+ or V β 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 β families (V β 1, V β 5, V β 8, V β 14, V β 16, V β 17, V β 18, V β 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.
Files in This Item:
T199501493.pdf Download
DOI
10.3349/ymj.1995.36.1.68
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Se Jong(김세종)
Lee, Soo Kon(이수곤)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/186408
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