Interleukin 1-dependent induction of both interleukin 2 secretion and interleukin 2 receptor expression by thymoma cells.
Interleukin 1-dependent induction of both interleukin 2 secretion and interleukin 2 receptor expression by thymoma cells.
复制标题
胸腺瘤细胞白细胞介素 1 依赖性诱导白细胞介素 2 分泌和白细胞介素 2 受体表达。
作者：
J. Lowenthal;J. Cerottini;H. Macdonald
巨噬细胞衍生的产物白细胞介素1（IL 1）被认为在T淋巴细胞的增殖中起重要的调节作用;然而，其作用机制尚不清楚。在这份报告中，我们描述了一个变体亚系的EL 4胸腺瘤细胞（EL 4 -6.1），显示出高度的反应性IL 1。结果表明，重组IL-1可诱导这些细胞分泌白细胞介素2（IL-2）和表达IL-2受体（IL-2-R）。EL 4 -6.1细胞不组成性分泌IL 2，也不表达IL 2-R;但当在重组IL 1存在下培养时，它们分泌可检测量的IL 2（5至15 U/ml）。在佛波酯（PMA）或离子霉素的存在下，添加IL 1导致IL 2分泌量增加80倍。IL 1单独或与离子霉素联合刺激不能诱导EL 4 6 1细胞表达可检测的IL 2 R。然而，在次优浓度的PMA存在下，IL 1诱导约3000高亲和力（解离常数，Kd为31 pM）和50，000低亲和力（Kd为2800 pM）IL 2-R的表达。这些IL 2-R是功能性的，基于它们快速内化IL 2的能力。该模型系统将允许详细分析IL 1和IL 2调节免疫应答的机制。
The macrophage-derived product, interleukin 1 (IL 1) is thought to play an important regulatory role in the proliferation of T lymphocytes; however, its mechanism of action is unknown. We describe in this report a variant subline of EL4 thymoma cells (EL4-6.1) that displays a high degree of responsiveness to IL 1. We show that recombinant IL 1 can induce both the secretion of interleukin 2 (IL 2) and the expression of IL 2 receptors (IL 2-R) by these cells. EL4-6.1 cells do not constitutively secrete IL 2, nor do they express IL 2-R; but when cultured in the presence of recombinant IL 1, they secrete detectable amounts of IL 2 (5 to 15 U/ml). In the presence of either suboptimal levels of phorbol ester (PMA) or Ionomycin, the addition of IL 1 resulted in up to an 80-fold enhancement in the amount of IL 2 secreted. Stimulation with IL 1 alone or in combination with Ionomycin was unable to induce detectable IL 2-R expression by EL4-6.1 cells. However, in the presence of suboptimal concentrations of PMA, IL 1 induced expression of about 3000 high affinity (dissociation constant, Kd of 31 pM) and 50,000 low affinity (Kd of 2800 pM) IL 2-R. These IL 2-R were functional, based on their ability to rapidly internalize IL 2. This model system will allow a detailed analysis of the mechanisms involved in the regulation of the immune response by IL 1 and IL 2.