Alterations in interleukin-2 utilization by T-cells from rats treated with an ethanol-containing diet.
Alterations in interleukin-2 utilization by T-cells from rats treated with an ethanol-containing diet.
复制标题
用含乙醇饮食处理的大鼠 T 细胞对白细胞介素 2 利用率的改变。
DOI：
10.1111/j.1530-0277.1990.tb00480.x
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Marietta,C
中科院分区：
文献类型：
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作者：
Jerrells,TR;Perritt,D;Eckardt,MJ;Marietta,C
Sprague-道利大鼠给予乙醇后，伴刀豆球蛋白A导致淋巴细胞增殖缺陷。由于T细胞增殖中的一个关键因素是白细胞介素-2的产生，因此设计实验以评价乙醇对乙醇处理动物脾细胞产生和利用白细胞介素-2的影响。为了确保脾细胞对促有丝分裂刺激反应的变化不是简单地由反应性T细胞的损失引起的，我们测试了尼龙毛非粘附细胞。从乙醇处理的大鼠中分离的T细胞对伴刀豆球蛋白A的反应始终低于来自对照动物的等量细胞。向T细胞培养物中添加重组白细胞介素-2并不能纠正乙醇处理大鼠细胞中发现的伴刀豆球蛋白A增殖缺陷。进一步的研究结果表明，乙醇处理动物的T细胞产生的白细胞介素-2等于或大于对照饲料动物的细胞。然而，从乙醇处理动物的伴刀豆球蛋白A刺激48小时的脾细胞培养物中回收的原始细胞显示出对外源性白细胞介素-2应答的增殖能力降低。在检测到高亲和力结合的条件下，125 I-白细胞介素-2与伴刀豆球蛋白A刺激产生的胚细胞的结合在处理动物和对照动物的细胞中相似。这些数据表明，乙醇处理动物的淋巴细胞增殖缺陷不是由T细胞缺乏白细胞介素-2产生引起的。同样明显的是，来自乙醇处理大鼠的T细胞不缺乏高亲和力白细胞介素-2受体。
Administration of ethanol to Sprague‐Dawley rats has been shown to produce a defect in lymphocyte proliferation in response to concanavalin A. Because a critical element in T‐cell proliferation is the production of interleukin‐2, experiments were designed to evaluate the influence of ethanol on the production and utilization of interleukin‐2 by spleen cells from ethanol‐treated animals. To ensure that changes in spleen cell responses to mitogenic stimulation were not simply caused by a loss of responding T cells, we tested nylon wool‐nonadherent cells. The response to concanavalin A of isolated T cells from ethanol‐treated rats was consistently less than that of equivalent numbers of cells from control animals. The addition of recombinant interleukin‐2 to cultures of T cells did not correct the defect in proliferation to concanavalin A noted in cells from ethanol‐treated rats. Further study results demonstrated that interleukin‐2 production by T cells from ethanol‐treated animals was equal to or greater than that by cells from animals given control diet. Blast cells recovered from 48‐hr concanavalin A‐stimulated spleen cell cultures from ethanol‐treated animals, however, showed a decreased ability to proliferate in response to exogenous interleukin‐2. Binding of125I‐interleukin‐2 to blast cells resulting from concanavalin A stimulation, under conditions that detected high‐affinity binding, was similar in cells from treated and control animals. These data indicate that the deficiency in proliferation of lymphocytes from ethanol‐treated animals is not caused by a lack of interleukin‐2 production by the T cells. It is also apparent that T cells from ethanol‐treated rats are not deficient in high‐affinity interleukin‐2 receptors.