Cohen H J
J Clin Invest. 1975 Jan;55(1):84-93. doi: 10.1172/JCI107921.
The phenomenon of redistribution of surface membrane immunoglobulin (Ig) components (capping) has been well described in mouse lymphoid cells. The characteristics of this process in human lymphocytes are less clear. This study characterizes the phenomenon of surface membrane Ig redistribution of normal and chronic lymphocytic leukemia (CLL) lymphocytes with the use of fluoroscein-labeled anti-Ig sera. Normal lymphocytes underwent rapid cap formation after incubation with anti-Ig serum in the cold and subsequent rewarming. The morphology was characteristic with aggregation over the pole of the cell opposite the nucleus and over the uropod when present. The process was energy dependent but independent of protein synthesis, and could be inhibited by vincristine, vinblastine, and colchicine but not by cytochalasin B. CLL cells, on the other hand, though showing fluorescent complex aggregation on the surface, rarely demonstrated unidirectional movement of these aggregates to form a cap. Cap formation in these cells could not be stimulated by supplementing the energy source or protein concentration of the medium nor by adding glutamic acid which could partially reverse the vincristine and vinblastine inhibition of normal capping. The failure of agents which inhibit motility to inhibit capping of the normal lymphocytes suggests that active locomotion is not a direct prerequisite for capping. The results also suggest the involvement of microtubules in normal capping and the possibility that abnormal membrane structure or microtubular function could explain the failure of CLL cells to behave normally in this regard. The role of this cellular defect in the immune deficiencies exhibited by many patients with CLL, however, is not established.
表面膜免疫球蛋白（Ig）成分重新分布（帽化）的现象在小鼠淋巴细胞中已有详尽描述。而这种过程在人类淋巴细胞中的特征尚不太明确。本研究利用荧光素标记的抗Ig血清，对正常淋巴细胞和慢性淋巴细胞白血病（CLL）淋巴细胞表面膜Ig重新分布的现象进行了特征描述。正常淋巴细胞在低温下与抗Ig血清孵育，随后复温后会迅速形成帽。其形态特征为在细胞核相对的细胞极以及存在尾足时在尾足上出现聚集。该过程依赖能量，但与蛋白质合成无关，并且可被长春新碱、长春花碱和秋水仙碱抑制，而不被细胞松弛素B抑制。另一方面，CLL细胞虽然在表面显示出荧光复合物聚集，但这些聚集物很少表现出单向移动以形成帽。通过补充培养基的能量来源或蛋白质浓度，或添加谷氨酸（其可部分逆转长春新碱和长春花碱对正常帽化的抑制），均无法刺激这些细胞形成帽。抑制运动的药物未能抑制正常淋巴细胞的帽化，这表明主动运动并非帽化的直接先决条件。结果还提示微管参与正常帽化，并且膜结构异常或微管功能异常可能解释CLL细胞在这方面表现异常的原因。然而，这种细胞缺陷在许多CLL患者所表现出的免疫缺陷中的作用尚未明确。
