Klaus G G, Hawrylowicz C M
Eur J Immunol. 1984 Mar;14(3):250-4. doi: 10.1002/eji.1830140309.
We have previously shown that cyclosporine (CS) selectively inhibits polyclonal activation of B cells by anti-Ig antibodies but not by lipopolysaccharide (LPS). Here we extend these results using a two-stage B cell culture system in which cells from either CBA/N or normal mice are activated to enter G1 by anti-Ig, and are then stimulated to proliferate by LPS. In this system CS blocks an event that occurs within 4 h after initial activation, i.e. prevents entry of B cells into G1. Phorbol myristic acetate also induces some CBA/N B cells to enter G1. However, activation of B cells by this agent is resistant to inhibition by CS. These data suggest that there are two biochemically distinct mechanisms for driving resting B cells into G1. A hypothesis to explain these results is presented.
我们之前已经表明，环孢素（CS）可选择性抑制抗Ig抗体对B细胞的多克隆激活，但对脂多糖（LPS）介导的激活无此作用。在此，我们使用两阶段B细胞培养系统扩展了这些结果，在该系统中，来自CBA/N小鼠或正常小鼠的细胞先通过抗Ig激活进入G1期，然后用LPS刺激其增殖。在这个系统中，CS阻断了初始激活后4小时内发生的一个事件，即阻止B细胞进入G1期。佛波酯也可诱导一些CBA/N B细胞进入G1期。然而，该试剂对B细胞的激活不受CS抑制。这些数据表明，存在两种将静止B细胞驱动进入G1期的生化机制不同的途径。本文提出了一个解释这些结果的假说。
