Melchers F, Corbel C, Leptin M, Lernhardt W
J Cell Sci Suppl. 1985;3:77-82. doi: 10.1242/jcs.1985.supplement_3.8.
The cell cycle of activated murine B lymphocytes (B cells) is controlled by the occupancy of surface membrane-bound immunoglobulin (Ig) and by two types of growth factors, called alpha and beta factors. These growth factors are produced in an endocrine fashion by the interaction of helper T lymphocytes (T cells) with antigen-presenting macrophages (A cells). Antigen is taken up, processed and presented on the surface of A cells in the context of class II major histocompatibility complex (MHC) glycoproteins. Helper T cells recognize this association of antigen and class II MHC molecules. A cells produce alpha factors and T cells produce beta factors. The molecular nature of these factors and of the corresponding receptors on B cells has yet to be elucidated, although it can be shown that the complement component C3d replaces alpha factor action. Resting, G0 phase B cells are refractory to the action of alpha and beta factors. They have to be excited, i.e. rendered susceptible to the action of these factors. This can be achieved by the interaction with helper T cells that recognize antigen, bound by surface membrane Ig, in the context of class II MHC glycoproteins on the surface of resting G0 B cells. Excitation can also occur in a polyclonal fashion by cross-linking of surface Ig with immobilized, Ig-specific antibodies, or by the interaction with polyclonal activators of B cells, such as lipopolysaccharides. Entry into the cell cycle is asynchronous. Activated, cycling B cells can be synchronized by size separation, using velocity sedimentation. Synchronized B cells will retain their synchrony for several divisions, when they are stimulated by immobilized Ig-specific antibodies, alpha and beta factors. They divide every 20 h at 37 degrees C. Omission of either of the three stimuli arrests B cells, though at different points in the cell cycle. Three restriction points are found: the first occurs immediately after mitosis and is controlled by the binding of immobilized Ig-specific antibodies to surface membrane-bound Ig.(ABSTRACT TRUNCATED AT 250 WORDS)
活化的小鼠B淋巴细胞（B细胞）的细胞周期受表面膜结合免疫球蛋白（Ig）的占据情况以及两种生长因子（称为α因子和β因子）的控制。这些生长因子以内分泌方式由辅助性T淋巴细胞（T细胞）与抗原呈递巨噬细胞（A细胞）相互作用产生。抗原在II类主要组织相容性复合体（MHC）糖蛋白的背景下被A细胞摄取、加工并呈递在其表面。辅助性T细胞识别抗原与II类MHC分子的这种结合。A细胞产生α因子，T细胞产生β因子。尽管可以证明补体成分C3d可替代α因子的作用，但这些因子以及B细胞上相应受体的分子性质尚未阐明。静止的G0期B细胞对α因子和β因子的作用具有抗性。它们必须被激活，即变得易于受到这些因子的作用。这可以通过与辅助性T细胞相互作用来实现，这些辅助性T细胞在静止的G0期B细胞表面的II类MHC糖蛋白背景下识别由表面膜Ig结合的抗原。激活也可以通过表面Ig与固定化的Ig特异性抗体交联，或以多克隆方式与B细胞的多克隆激活剂（如脂多糖）相互作用而发生。进入细胞周期是不同步的。活化的、处于周期中的B细胞可以通过速度沉降进行大小分离来实现同步化。当用固定化的Ig特异性抗体、α因子和β因子刺激时，同步化的B细胞在几个分裂周期内将保持同步。它们在37℃下每20小时分裂一次。省略这三种刺激中的任何一种都会使B细胞停滞，尽管停滞在细胞周期的不同点。发现了三个限制点：第一个发生在有丝分裂后立即，由固定化的Ig特异性抗体与表面膜结合Ig的结合控制。
