Tagawa S, Hatakeyama M, Shibano M, Taniguchi T, Kitani T
Department of Clinical Research, Osaka University, Japan.
Blood. 1988 Apr;71(4):1161-4.
The expression of interleukin 2 receptor (IL-2R) on leukemic cells of natural killer (NK) and T cell lineages in two patients with large granular lymphocytic (LGL) leukemia was examined. The p55 Tac IL-2R was not detected by the indirect immunofluorescence method and it did not participate in the IL-2 binding to the surface of these cells. However, these leukemic cells proliferated in a IL-2 dose-dependent manner and expressed p55. A p75 IL-2 receptor (IL-2-R) subunit was detected on the LGL leukemic cells of both NK and T lineages in a crosslink assay. Thus, it is suggested that the primary signal of IL-2 is mediated by the p75 alone. A study of the inhibitions of the proliferative response of LGL leukemia cells by anti-Tac revealed that both p75 and secondarily induced p55 are required for the cell proliferation.
检测了两名大颗粒淋巴细胞（LGL）白血病患者自然杀伤（NK）和T细胞系白血病细胞上白细胞介素2受体（IL-2R）的表达。间接免疫荧光法未检测到p55 Tac IL-2R，且其不参与IL-2与这些细胞表面的结合。然而，这些白血病细胞以IL-2剂量依赖的方式增殖并表达p55。在交联试验中，在NK和T系的LGL白血病细胞上均检测到p75 IL-2受体（IL-2-R）亚基。因此，提示IL-2的主要信号仅由p75介导。抗Tac对LGL白血病细胞增殖反应抑制作用的研究表明，细胞增殖需要p75和继发性诱导的p55。
