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Increased Expression of Down‐Regulatory CTLA‐4 Molecule on T Lymphocytes from Rheumatoid Synovial Compartment
Author(s) -
Ming Fei Liu,
Chuning Yang,
Jinfeng Li,
Kenneth Lai,
SheauChiou Chao,
HuanYao Lei
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00565.x
Subject(s) - ctla 4 , rheumatoid arthritis , tumor necrosis factor alpha , synovial fluid , immunology , synovial membrane , medicine , t cell , inflammation , peripheral blood mononuclear cell , rheumatoid factor , antibody , chemistry , immune system , pathology , in vitro , biochemistry , alternative medicine , osteoarthritis
Since the CTLA‐4 molecule expressed on activated T lymphocytes has recently been suggested to be an important negative regulator in autoimmune diseases, this study was undertaken to investigate the expression and function of CTLA‐4 on synovial T cells from patients with rheumatoid arthritis. CTLA‐4‐expressing T cells were detected using a dual fluorescence flow cytometric method. Only a small percentage of peripheral blood T cells from patients with rheumatoid arthritis had detectable surface CTLA‐4 expression (mean ± SD, 1.89 ± 1.92%). However, the levels of CTLA‐4‐positive T cells was increased significantly in rheumatoid synovial fluids (5.44 ± 4.96%) and synovial membranes (28.76 ± 14.30%). To explore the role of CTLA‐4 molecule in the inflammation of rheumatoid joints, CTLA‐4 was blocked with anti‐CTLA‐4 antibody to assess its effects on the production of tumour necrosis factor α and interleukin 1β in synovial fluid mononuclear cell culture. The addition of anti‐CTLA‐4 antibody enhanced the production of tumour necrosis factor α and interleukin 1β in a dose‐dependent manner. The data suggest that the expression of CTLA‐4 plays a down‐regulatory role in rheumatoid articular inflammation. We thus concluded that CTLA‐4 was up‐regulated on synovial T cells from patients with RA, and the increased CTLA‐4 expression might exert a down‐regulation effect on tumour necrosis factor α and interleukin 1β production.