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锂对小鼠应激诱导的细胞介导免疫抑制的保护作用。

Protective effect of lithium on the stress-induced depression of cell-mediated immunity in mice.

作者信息

Bubak-Satora M, Skowron-Cendrzak A, Kubera M, Holán V

机构信息

Department of Immunobiology, Polish Academy of Sciences, Krakow.

出版信息

Int J Immunopharmacol. 1994 Mar;16(3):233-7. doi: 10.1016/0192-0561(94)90017-5.

DOI:10.1016/0192-0561(94)90017-5
PMID:8206689
Abstract

The effect of lithium chloride (LiCl) administration on the stress-induced depression of cell-mediated immunity was studied in mice. Two models of stress-induced depression of immunity were used: (1) keeping the animals at a temperature of 4 degrees C twice for 24 h at a 24-h interval, and (2) keeping them in the dark for 96 h. Both kinds of stress significantly decreased the reactivity of cell donors in the graft-versus-host (GVH) reaction and recipients in the host-versus-graft (HVG) reaction. Treatment with LiCl of the cell donors in GVH reaction or the recipients in HVG reaction daily for three weeks before stress application completely abolished the immunosuppressive effect of "cooling" stress, but not "darkness" stress. The LiCl is thus shown as a potential immunomodulator protecting mice from some forms of the stress-induced depression of cell-mediated immunity.

摘要

研究了氯化锂(LiCl)给药对小鼠应激诱导的细胞介导免疫抑制的影响。使用了两种应激诱导免疫抑制的模型:(1)将动物在4摄氏度的温度下间隔24小时保持两次,每次24小时;(2)将它们置于黑暗中96小时。两种应激均显著降低了移植物抗宿主(GVH)反应中细胞供体以及宿主抗移植物(HVG)反应中受体的反应性。在施加应激前三周,每天对GVH反应中的细胞供体或HVG反应中的受体用LiCl进行处理,完全消除了“冷却”应激的免疫抑制作用,但未消除“黑暗”应激的免疫抑制作用。因此,LiCl被证明是一种潜在的免疫调节剂,可保护小鼠免受某些形式的应激诱导的细胞介导免疫抑制。

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