Maeda Y, Hattori T, Sakai K, Yamamura Y, Murakami T, Asou N, Tsudo M, Takatsuki K
Second Department of Internal Medicine, Kumamoto University Medical School, Japan.
Growth Factors. 1991;4(4):289-95. doi: 10.3109/08977199109043914.
Monoclonal antibodies, each recognizing interleukin 2 receptor (IL-2R) alpha, or beta, were used to see the regulatory mechanisms of the expressions on leukemic cells from a patient with T4 chronic lymphocytic leukemia (T4-CLL). Cells from this patient expressed only IL-2R beta, and the expression was enhanced by medium cultivation. IL-1 enhanced the expression of not only IL-2R beta but also IL-2R alpha on the cells. Binding studies using 125I-IL-2 showed the presence of an intermediate receptor (734 sites/cell, Kd = 1.2 nM) and a few high-affinity receptor (172 sites/cell, Kd = 132 pM) on cells cultured with IL-1. IL-2 and IL-1 synergistically promoted the proliferation of the cells, suggesting that the induced IL-2R was functional. In addition, anti-IL-1 antibodies inhibited IL-2R beta expression by cultured cells, suggesting that it was dependent on IL-1 produced by the leukemic cells. These findings suggested that IL-1 might enhance the expression of IL-2R beta in a subset of human T cells, and implied a role of IL-1 in the proliferation of the leukemic T cells.
使用分别识别白细胞介素2受体（IL-2R）α或β的单克隆抗体，来研究一名T4慢性淋巴细胞白血病（T4-CLL）患者白血病细胞上这些受体表达的调控机制。该患者的细胞仅表达IL-2Rβ，并且通过培养基培养可增强其表达。IL-1不仅增强了细胞上IL-2Rβ的表达，还增强了IL-2Rα的表达。使用125I-IL-2进行的结合研究表明，在用IL-1培养的细胞上存在一种中间受体（734个位点/细胞，Kd = 1.2 nM）和一些高亲和力受体（172个位点/细胞，Kd = 132 pM）。IL-2和IL-1协同促进细胞增殖，表明诱导产生的IL-2R具有功能。此外，抗IL-1抗体抑制培养细胞的IL-2Rβ表达，表明其表达依赖于白血病细胞产生的IL-1。这些发现提示IL-1可能增强人类T细胞亚群中IL-2Rβ的表达，并暗示IL-1在白血病T细胞增殖中起作用。
