Correction of interleukin-2 production in patients with systemic lupus erythematosus by removal of spontaneously activated suppressor cells.
Correction of interleukin-2 production in patients with systemic lupus erythematosus by removal of spontaneously activated suppressor cells.
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通过去除自发激活的抑制细胞来纠正系统性红斑狼疮患者白细胞介素 2 的产生。
DOI：
10.1172/jci111758
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Horwitz,DA
中科院分区：
文献类型：
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作者：
Linker-Israeli,M;Bakke,AC;QuismorioJr,FP;Horwitz,DA
系统性红斑狼疮（SLE）患者体外白细胞介素-2（IL-2）的产生受到抑制。目前尚不清楚这种异常是由生产淋巴细胞的缺陷或过度抑制引起的。我们报告，OKT 8（Leu 2a）+细胞的去除增加了IL-2的生产在体外刺激淋巴细胞正常或高于正常水平的21例SLE患者中的19。这种增加在临床非活动性疾病和/或接受少于7.5 mg泼尼松的患者中更为明显。从正常人中去除OKT 8+细胞并没有显著增加IL-2活性。SLE，但不是正常的，OKT 8+细胞减少IL-2的生产时，添加回自体OKT 8-耗尽的细胞。在一些实验中，来自正常供体的OKT 8+细胞也抑制SLE中IL-2的产生。这一结果表明，IL-2产生的缺陷是复杂的，可能涉及多个细胞的相互作用。三条证据表明SLE OKT 8+细胞主动抑制IL-2的产生，而不是被动吸收这种淋巴因子：（a）用抗Tac检测到只有3.2%的SLE淋巴细胞表达IL-2受体;（B）新鲜制备的SLE淋巴细胞不吸收IL-2;（c）SLE OKT 8+细胞的无细胞上清液抑制IL-2的产生，但不抑制IL-2的活性。流式细胞术双标记研究显示，19.3%的SLE OKT 8+细胞也是Ia阳性，约33%共表达自然杀伤细胞标志物HNK-1（Leu 7）。去除Leu 7+细胞也显著提高SLE中IL-2的产生。这些研究表明，SLE患者的一个或多个循环单核细胞亚群可以抑制IL-2的产生，其中一个亚群可能属于非T、非B“第三单核细胞群。"
Interleukin-2 (IL-2) production in vitro is depressed in systemic lupus erythematosus (SLE) patients. It is not known whether this abnormality is caused by a defect in the producer lymphocytes or by excessive suppression. We report that removal of OKT8 (Leu 2a)+ cells increased the IL-2 production by in vitro-stimulated lymphocytes to normal or above normal levels in 19 of 21 SLE patients. This increase was more apparent in those patients with clinically inactive disease and/or receiving less than 7.5 mg of prednisone. Removal of OKT8+ cells from normals did not significantly increase IL-2 activity. SLE, but not normal, OKT8+ cells decreased IL-2 production when added back to autologous OKT8-depleted cells. In some experiments, OKT8+ cells from normal donors also suppressed IL-2 production in SLE. This result suggests that the defect in IL-2 production is complex and may involve multiple cell interactions. Three lines of evidence suggest that the SLE OKT8+ cells actively inhibit the production of IL-2 rather than passively absorb this lymphokine: (a) only 3.2% of SLE lymphocytes expressed IL-2 receptors as detected with anti-Tac; (b) freshly prepared SLE lymphocytes did not absorb IL-2; and (c) cell-free supernatants from SLE OKT8+ cells inhibited IL-2 production, but not IL-2 activity. Double-labeling studies by flow cytometry revealed that 19.3% of SLE OKT8+ cells were also Ia-positive, and approximately 33% co-expressed the natural killer cell marker, HNK-1 (Leu 7). Removal of Leu 7+ cells also significantly elevated IL-2 production in SLE. These studies suggest that one or more circulating mononuclear cell subsets in SLE patients can suppress IL-2 production and that one subset may possibly belong to a non-T, non-B "third mononuclear population."