Volume 25, Issue 12 pp. 3243-3248
Article
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Role of tumor necrosis factor-α in the regulation of activated synovial T cell growth: Downregulation of synovial T cells in rheumatoid arthritis patients

Ning-Sheng Lai

Ning-Sheng Lai

Section of Allergy, Immunology and Rheumatology, Department of Medicine, Veterans General Hospital-Taichung, Taichung, Taiwan, R.O.C

Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C

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Joung-Liang Lan

Joung-Liang Lan

Section of Allergy, Immunology and Rheumatology, Department of Medicine, Veterans General Hospital-Taichung, Taichung, Taiwan, R.O.C

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Chia-Li Yu

Chia-Li Yu

Section of Allergy, Immunology and Rheumatology, Department of Medicine, Veterans General Hospital-Taipei, National Yang Ming University, Taipei, Taiwan, R.O.C

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Rong-Hwa Lin

Corresponding Author

Rong-Hwa Lin

Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C

Graduate Institute of Immunology, College of Medicine, National Taiwan University, No. 1., Sec. 1., Jen AiRd., Taipei, Taiwan, R.O.C. (Fax: +886-2-321-7921)Search for more papers by this author
First published: December 1995
Citations: 7

Abstract

To characterize the role of tumor necrosis factor (TNF)-α in regulating synovial T cell growth, cell cycle progression associated with TNF-α in mitogen-activated synovial T cells of patients with rheumatoid arthritis (RA) were analyzed. After mitogen stimulation, the majority of synovial T cells in RA patients accumulated in S-phase. Anti-human TNF-α monoclonal antibody and soluble recombinant human TNF receptor (rhTNFR) can block S-phase accumulation. Furthermore, synovial fluid (SF) from RA patients was able to inhibit the proliferation of these S-phase-accumulated T cells. These data indicate that TNF-α could regulate activated synovial T cell growth by driving them into S-phase. Combined with the activities of other components of SF, TNF-α seems to play an important role in down-regulating activated synovial T cells in RA patients. In addition, the elevated level of soluble TNFR in the SF of disease-active RA patients is believed to be associated with the promotion of synovial T cell responses.

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