Lymphoma models for B cell activation and tolerance. III. Cell cycle dependence for negative signalling of WEHI-231 B lymphoma cells by anti-mu.
Lymphoma models for B cell activation and tolerance. III. Cell cycle dependence for negative signalling of WEHI-231 B lymphoma cells by anti-mu.
复制标题
DOI：
10.1084/jem.164.1.156
复制
发表时间：
1986-07-01
期刊：
影响因子：
--
通讯作者：
Keng P
中科院分区：
文献类型：
--
作者：
Scott DW;Livnat D;Pennell CA;Keng P
WEHI-231B淋巴瘤细胞已被证明是抗Ig试剂调节正常B细胞生长的有用模型。我们以前报道过，这些淋巴瘤细胞的生长被异源或单抗Mu或抗kappa试剂抑制。这些细胞在24-48小时内停止结合胸腺嘧啶核苷，但不会受到针对I类或II类组织相容性抗原的抗体的不利影响。事实上，细胞周期分析显示，抗Mu抗体导致这些细胞从G1期向S期的转变受阻。为了进一步研究细胞生长抑制的机制，我们用离心洗脱法纯化了G1期淋巴瘤细胞，或用羟基脲处理浓缩了G1/S界面上的WEHI231细胞，并在有或没有抗MU抗体的情况下观察了它们在细胞周期中的进展。我们的数据显示，WEHI-231B淋巴瘤细胞在G1期早期收到负信号，因为延迟加入抗MU(对G1晚期细胞)在24小时时不会导致细胞周期的变化，在S期间暴露于抗MU不会改变DNA合成和有丝分裂的进展。此外，仅在抗MU抗体作用2小时后，纯化的G1细胞就不能进入第一个S时相。从B细胞活化和耐受诱导模型的角度讨论了G1期早期相关过程的本质。
WEHI-231 B lymphoma cells have proven to be a useful model for the regulation of growth of normal B cells by anti-Ig reagents. We previously reported that the growth of these lymphoma cells is inhibited by heterologous or monoclonal anti-mu or anti-kappa reagents. Such cells cease to incorporate thymidine within 24-48 h of exposure to anti-Ig reagents, but are not adversely affected by antibodies directed at either class I or class II histocompatibility antigens. In fact, cell cycle analysis revealed that anti-mu causes a block in the transition of these cells from G1 to S phase. To further study the mechanism of growth inhibition, we have purified lymphoma cells in G1 by centrifugal elutriation, or enriched WEHI-231 cells at the G1/S interface by treatment with hydroxyurea, and followed their progression through the cell cycle in the presence or absence of anti-mu. Our data show that WEHI-231 B lymphoma cells receive a negative signal early in G1, since delayed addition of anti-mu (to late G1 cells) leads to no alteration in cell cycle progression at 24 h, and exposure to anti-mu during S does not alter progress through DNA synthesis and mitosis. Moreover, exposure to anti-mu for only 2 h prevents purified G1 cells from entering their first S phase. The nature of the relevant processes in early G1 is discussed in terms of models of B cell activation and tolerance induction.