Katagiri K, Nakano T, Sugawara Y, Ichikawa Y, Yoshida T
Tokyo Institute for Immunopharmacology, Inc., Japan.
Clin Immunol Immunopathol. 1990 Sep;56(3):384-92. doi: 10.1016/0090-1229(90)90158-m.
The effect of the anti-rheumatic drug CCA (disodium 4-chloro-2,2'-iminodibenzoate) on the proliferation of T cells activated by PHA was examined. Cell cycle analysis showed that CCA blocked the transition of the cells from G1 to S (progression), but had little effect on the G0----G1 transition (initiation). CCA had no significant effect on IL-2 receptor expression, an early G1 event, but did inhibit transferrin receptor expression, a late G1 event. CCA did not inhibit IL-2 production by PHA-activated T cells, but did block IFN-gamma production at 72 hr after the stimulation. CCA failed to inhibit c-myc mRNA induction, but did delay the decrease in c-myc mRNA levels that normally occurs with the onset of DNA synthesis. These results indicate that CCA inhibits the progression, but not initiation, of human T cell proliferation.
研究了抗风湿药物CCA（4-氯-2,2'-亚氨基二苯甲酸二钠）对PHA激活的T细胞增殖的影响。细胞周期分析表明，CCA阻断了细胞从G1期到S期的转变（进展），但对G0期到G1期的转变（起始）影响很小。CCA对IL-2受体表达（G1期早期事件）无显著影响，但确实抑制了转铁蛋白受体表达（G1期晚期事件）。CCA不抑制PHA激活的T细胞产生IL-2，但在刺激后72小时确实阻断了IFN-γ的产生。CCA未能抑制c-myc mRNA的诱导，但确实延迟了DNA合成开始时正常发生的c-myc mRNA水平的下降。这些结果表明，CCA抑制人T细胞增殖的进展，但不抑制起始。
