Leuther M D, Peacock J S, Krakauer H, Barisas B G
J Immunol. 1981 Sep;127(3):893-9.
Changes in lateral mobilities of rabbit lymphocyte membrane components in response to succinyl concanavalin A (S Con A) have been studied by fluorescence photobleaching recovery (FPR). During hrs 0 to 3 after exposure to S Con A, lectin receptor mobilities on both T and B cells fall about 2-fold. Reduced mobility of T cell lectin receptors persists until hr 18. From hr 18 to 24 rapid recovery of original mobility occurs if and only if lectin is present. In contrast, nonresponding B cells recover original receptor mobility gradually over hr 4 to 48. Metabolic inhibitors added at hr 3 restore original receptor mobilities, but cytoskeletal disruptors have this effect on T cells only. From hr 0 to 15, washing lectin from the cell surface is decreasingly effective in restoring T cell receptor mobility. After hr 15, mobility cannot be enhance by lectin removal. Parallel DNA synthesis studies show that, for T cell stimulation, lectin must be present on the cell surface during hr 0 to 3 and 18 to 24. These are the periods when FPR measurements show lectin receptor mobilities being restricted and released, respectively. Stimulation of B cells by anti-Ig shows several interesting features. First, stimulation by intact anti-Ig fails to reduce the mobilities of Con A receptors in a manner similar to that produced by S Con A. Second, S Con A does reduce mobility of surface Ig. Thus, Con A receptors would appear to exert a unique anchorage modulation of mobilities of other membrane molecules.
通过荧光光漂白恢复技术(FPR)研究了兔淋巴细胞膜成分对琥珀酰伴刀豆球蛋白A(S Con A)的侧向流动性变化。在暴露于S Con A后的0至3小时内,T细胞和B细胞上的凝集素受体流动性均下降约2倍。T细胞凝集素受体的流动性降低一直持续到18小时。从18小时到24小时,只有当凝集素存在时,原始流动性才会快速恢复。相比之下,无反应的B细胞在4至48小时内逐渐恢复原始受体流动性。在3小时添加代谢抑制剂可恢复原始受体流动性,但细胞骨架破坏剂仅对T细胞有此作用。从0小时到15小时,从细胞表面洗去凝集素恢复T细胞受体流动性的效果逐渐降低。15小时后,去除凝集素不能提高流动性。平行的DNA合成研究表明,对于T细胞刺激,凝集素必须在0至3小时和18至24小时存在于细胞表面。这正是FPR测量分别显示凝集素受体流动性受到限制和释放的时期。抗Ig对B细胞的刺激表现出几个有趣的特征。首先,完整抗Ig的刺激未能以类似于S Con A产生的方式降低Con A受体的流动性。其次,S Con A确实会降低表面Ig的流动性。因此,Con A受体似乎对其他膜分子的流动性发挥独特的锚定调节作用。