BETA-ENDORPHIN MODULATION OF IL-1-INDUCED IL-2 PRODUCTION
BETA-ENDORPHIN MODULATION OF IL-1-INDUCED IL-2 PRODUCTION
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DOI：
10.1016/0162-3109(90)90021-6
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发表时间：
1990-01-01
期刊：
影响因子：
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通讯作者：
SERRATE, SA
中科院分区：
文献类型：
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作者：
BESSLER, H;SZTEIN, MB;SERRATE, SA
我们研究了天然阿片类物质对淋巴细胞系EL-4产生白细胞介素-1（IL-1）诱导的白细胞介素2（IL-2）的影响。β-的内啡肽（β- end）显著增强IL-1刺激的EL-4细胞产生IL-2。使用LBRM 33 - 1A 5细胞系获得了类似的结果。β-的在所有测试的IL-1浓度（2-0.25 U/ml）下，End诱导了IL-1诱导的IL-2产生的显著增强（35-100%），并且用两种IL-1 α都观察到了效果。和IL-1 β。β的剂量反应IL-1诱导的IL-2产生的末端增强是双峰的，在高（10-8-10-10 M）和低（10-16 M）β-浓度下观察到峰值活性。终浓度。β的特异性-使用阿片样物质拮抗剂纳洛酮研究终末效应。纳洛酮完全消除了β-结果表明，这种作用可能是通过与阿片受体结合而介导的。此外，其它阿片肽，包括γ-内啡肽和脑啡肽引起了类似的效果。北方印迹分析显示，在β-IFN-γ细胞中IL-2 mRNA的水平更高。终末处理的IL-1诱导的EL-4细胞比IL-1诱导的对照细胞中的细胞增殖。因此，β-末端可能通过增加转录速率或增加IL-2 mRNA稳定性来增强IL-2的产生。这些结果表明，β-除了已知的在中枢神经系统中与IL-1的相互作用外，末端可能在外周淋巴因子产生的调节中起重要作用。
We have studied the effects of natural opioids on interleukin-1 (IL-1) -induced interleukin 2 (IL-2) production by the lymphoid cell line EL-4. .beta.-Endorphin (.beta.-end) significantly enhanced IL-2 production by IL-1-stimulated EL-4 cells. Similar results were obtained using the LBRM33-1A5 cell line. .beta.-End induced significant enhancement (35-100%) of IL-1-induced IL-2 production at all concentrations of IL-1 tested (2-0.25 U/ml) and the effects were seen with both IL-1.alpha. and IL-1.beta.. The dose response of .beta.-end augmentation of IL-1-induced IL-2 production was bimodal, with peak activities seen at high (10-8-10-10 M) and low (10-16 M) .beta.-end concentrations. The specificity of .beta.-end effect was studied using the opioid antagonist naloxone. Naloxone completely abolished the enhancing effects of .beta.-end, indicating that the effects might be mediated through binding to opioid receptors. In addition, other opioid peptides, including .gamma.-endorphin and enkephalins, elicited similar effects. Northern blotting analysis revealed higher levels of IL-2 mRNA in .beta.-end-treated IL-1-induced EL-4 cells than in IL-1-induced control cells. Thus, .beta.-end might enhance IL-2 production by either augmenting the transcription rate or increasing IL-2 mRNA stability. These results suggest that .beta.-end might play an important role in the regulation of lymphokine production in the periphery in addition to its known interactions with IL-1 in the central nervous system.