作者: M. KLOPPENBURG , C. L. VERWEIJ , A. M. M. MILTENBURG , A. J. VERHOEVEN , M. R. DAHA
DOI: 10.1111/J.1365-2249.1995.TB03864.X
关键词:
摘要: Minocycline has been shown to have an anti-inflammatory effect in patients with rheumatoid arthritis (RA). Since there is evidence that RA a T cell-mediated disease, we investigated the of minocycline on human cell clones derived from synovium patient. The cells, when activated via receptor (TCR)/CD3 complex, were suppressed functionally by minocycline, resulting dose-dependent inhibition proliferation and reduction production IL-2, interferon-gamma (IFN-gamma) tumour necrosis factor-alpha (TNF-alpha). Besides IL-2 production, exerted its induction decreased responsiveness. We showed chelating capacity plays crucial role inhibitory function, since could be annulled addition exogenous Ca2+. However, did not markedly influence typical TCR/CD3-induced intracellular Ca2+ mobilization. Taken together, results clearly indicate immunomodulating effects cells.