Dunlap J E, Nichols W S, Hebebrand L C, Mathes L E, Olsen R G
Cancer Res. 1979 Mar;39(3):956-8.
The virus-associated depression of concanavalin A mitogenesis which accompanies feline leukemia virus-induced cat lymphoma was investigated by comparing lymphocyte surface receptor mobility of normal cats to that of viremic diseased animals. The mechanics of feline lymphocyte receptor mobility were studied using fluorescein-conjugated concanavalin A to quantitate lymphocyte capping. The results of a study of 21 disease-free animals showed that cat lymphocytes undergo appreciable concanavalin A capping, with a mean capping rate of 17% under conditions developed in this study. In contrast, morphologically normal peripheral blood lymphocytes of six feline leukemia virus-infected viremic cats, with or without lymphoma, exhibited a mean capping of only 7%, significantly less than that of the control animals (p less than 0.005). These findings suggest that a membrane-related lymphocyte deficiency accompanies the development of virus-induced lymphoma in the cat.
通过比较正常猫与病毒血症患病动物的淋巴细胞表面受体流动性,对猫白血病病毒诱导的猫淋巴瘤所伴随的伴刀豆球蛋白A有丝分裂的病毒相关性抑制进行了研究。使用荧光素偶联的伴刀豆球蛋白A来定量淋巴细胞帽化,研究了猫淋巴细胞受体流动性的机制。对21只无病动物的研究结果表明,猫淋巴细胞会发生明显的伴刀豆球蛋白A帽化,在本研究建立的条件下平均帽化率为17%。相比之下,6只感染猫白血病病毒的病毒血症猫(无论有无淋巴瘤)的形态正常外周血淋巴细胞平均帽化率仅为7%,显著低于对照动物(p小于0.005)。这些发现表明,在猫中,病毒诱导的淋巴瘤发展伴随着与膜相关的淋巴细胞缺陷。