Segel G B, Lichtman M A
J Cell Physiol. 1977 Nov;93(2):277-84. doi: 10.1002/jcp.1040930213.
Human blood T-lymphocytes increase their potassium (K+) permeability and active K+ transport following lectin or antigen stimulation. We have studied the permeability and active transport of K+ by lymphocytes in chronic lymphocytic leukemia (CLL) to determine if their membrane K+ transport was similar to resting or lectin-stimulated normal blood lymphocytes. K+ transport was assessed both by the rate of isotopic 42K+ uptake and by the rate of change in cell K+ concentration after inhibition of the K+ transport system with ouabain. CLL lymphocytes had a marked decrease in membrane K+ permeability and active transport of K+ when compared to blood T lymphocytes. K+ transport in five subjects with CLL (10 mmol.1 cell water-1.h-1) was half that in normal blood T-lymphocytes (20 mmol.1 cell water-1 h-1). Phytohemagglutinin (PHA) treatment of CLL lymphocytes did not increase significantly their active K+ transport, whereas K+ transport by normal T-lymphocytes increased by 100%. Since there were 73% T-lymphocytes in normal blood and 14% in CLL blood, the difference in membrane K+ turnover could be related either to neoplasia or to the proposed B-lymphocyte origin of CLL. We studied human tonsillar lymphocytes which contained a mean of 34% T-cells. In five studies of tonsils, K+ transport was 14 mmol.1 cell water-1.h-1 and treatment with PHA increased K+ transport only 30%. The intermediate values of basal K+ transport and K+ transport in response to PHA in tonsillar lymphocytes were consistent with the proportion of T-lymphocytes present. These data suggest that B-lymphocytes have reduced membrane permeability and active transport of K+. Thus the marked decrease in CLL lymphocyte membrane K+ permeability and transport may be a reflection of its presumed B-cell origin, rather than a membrane alteration related to malignant transformation.
人血T淋巴细胞在凝集素或抗原刺激后会增加其钾离子（K+）通透性和主动K+转运。我们研究了慢性淋巴细胞白血病（CLL）患者淋巴细胞的K+通透性和主动转运，以确定其膜K+转运是否与静息或凝集素刺激的正常血淋巴细胞相似。通过同位素42K+摄取速率以及用哇巴因抑制K+转运系统后细胞K+浓度的变化速率来评估K+转运。与血T淋巴细胞相比，CLL淋巴细胞的膜K+通透性和K+主动转运明显降低。5例CLL患者的K+转运（10 mmol·1细胞水-1·h-1）仅为正常血T淋巴细胞（20 mmol·1细胞水-1·h-1）的一半。用植物血凝素（PHA）处理CLL淋巴细胞并未显著增加其主动K+转运，而正常T淋巴细胞的K+转运增加了100%。由于正常血中T淋巴细胞占73%，CLL血中占14%，膜K+周转率的差异可能与肿瘤形成或CLL推测的B淋巴细胞起源有关。我们研究了平均含有34% T细胞的人扁桃体淋巴细胞。在对扁桃体的5项研究中，K+转运为14 mmol·1细胞水-1·h-1，用PHA处理后K+转运仅增加30%。扁桃体淋巴细胞基础K+转运及对PHA反应的K+转运的中间值与存在的T淋巴细胞比例一致。这些数据表明B淋巴细胞的膜通透性和K+主动转运降低。因此，CLL淋巴细胞膜K+通透性和转运的显著降低可能反映了其推测的B细胞起源，而非与恶性转化相关的膜改变。
