International Immunology, Vol. 12, No. 2, 187-193,
February 2000
© 2000 Japanese Society for Immunology
IL-6 inhibits the proliferation of fibroblastic synovial cells from rheumatoid arthritis patients in the presence of soluble IL-6 receptor
Department of Medical Science I, School of Health and Sport Sciences, Osaka University, 2-1 Yamadaoka, Suita-city, Osaka 565-0871, Japan
1 Department of Orthopedics, Osaka University Medical School, Osaka 565-0871, Japan
Correspondence to: K. Yoshizaki
IL-6 and tumor necrosis factor (TNF)-
have been proven to play an important role in the development of rheumatoid arthritis (RA). It is well known that TNF- induces IL-6 production from synovial cells as well as their proliferation. The effect of IL-6 on synovial cells, however, is not clear. An in vitrostudy was performed to determine the effect of IL-6 on the proliferation of synovial cells. Fibroblastic synovial cells isolated from the synovial tissues of eight RA patients were employed after the third to sixth passages. IL-6 in the presence of soluble IL-6 receptor (sIL-6R) inhibited the proliferation of synovial cells in a dose-dependent manner in seven cases without increasing the number of necrotic or apoptotic cells, while TNF- increased synovial cell proliferation in all cases. The inhibitory effect of IL-6 was observed only in the presence of sIL-6R although small amounts of IL-6R were detected in these cells by RT-PCR analysis. However, anti-IL-6R or anti-gp130 mAb treatment increased spontaneous growth of synovial cells in all eight cases, suggesting that endogenous IL-6 and a small amount of IL-6R expressed in synovial cells suppressed their growth without exogenous IL-6 or sIL-6R. In addition, the IL-6–sIL-6R complex reduced the TNF--induced proliferation of synovial cells while TNF- induced their IL-6 production. These data suggest that IL-6 may act as a negative feedback factor for TNF--induced synovial cell growth.
Keywords: IL-6, rheumatoid arthritis, soluble IL-6 receptor, synovial cell, tumor necrosis factor-
Transmitting editor: K. Okumura
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