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2
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本文引用的文献

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The differential expression of heat shock proteins in rheumatic disease.热休克蛋白在风湿性疾病中的差异表达。
Br J Rheumatol. 1993 Oct;32(10):883-92. doi: 10.1093/rheumatology/32.10.883.
2
Elevation of heat shock protein synthesis and hsp gene transcription during monocyte to macrophage differentiation of U937 cells.U937细胞从单核细胞向巨噬细胞分化过程中热休克蛋白合成及热休克蛋白基因转录的升高。
Clin Exp Immunol. 1993 Aug;93(2):178-83. doi: 10.1111/j.1365-2249.1993.tb07962.x.
3
Induction of heat-shock proteins by bacterial toxins, lipid mediators and cytokines in human leukocytes.细菌毒素、脂质介质和细胞因子在人白细胞中诱导热休克蛋白的产生。
Zentralbl Bakteriol. 1993 Apr;278(2-3):365-76. doi: 10.1016/s0934-8840(11)80853-4.
4
Differential heat shock protein overexpression and its clinical relevance in systemic lupus erythematosus.系统性红斑狼疮中热休克蛋白的差异过表达及其临床意义
Ann Rheum Dis. 1993 Jun;52(6):436-42. doi: 10.1136/ard.52.6.436.
5
Elevated levels of the 70 kD heat shock protein in patients with systemic lupus erythematosus are not dependent on enhanced transcription of the hsp70 gene.系统性红斑狼疮患者体内70 kD热休克蛋白水平升高并非依赖于hsp70基因转录增强。
Lupus. 1993 Oct;2(5):297-301. doi: 10.1177/096120339300200504.
6
Elevated levels of the 90 kD heat shock protein in patients with systemic lupus erythematosus are dependent upon enhanced transcription of the hsp90 beta gene.系统性红斑狼疮患者体内90 kD热休克蛋白水平升高，这取决于hsp90β基因转录的增强。
J Autoimmun. 1993 Aug;6(4):495-506. doi: 10.1006/jaut.1993.1041.
7
Elevation of the 90 kDa heat-shock protein in specific subsets of systemic lupus erythematosus.系统性红斑狼疮特定亚群中90 kDa热休克蛋白的升高。
Q J Med. 1994 Apr;87(4):215-22.
8
The tissue specific elevation in synthesis of the 90 kDa heat shock protein precedes the onset of disease in lupus prone MRL/lpr mice.在易患狼疮的MRL/lpr小鼠中，90 kDa热休克蛋白合成的组织特异性升高先于疾病发作。
J Rheumatol. 1994 Feb;21(2):234-8.
9
The interleukin-6-activated acute-phase response factor is antigenically and functionally related to members of the signal transducer and activator of transcription (STAT) family.白细胞介素-6激活的急性期反应因子在抗原性和功能上与信号转导及转录激活因子（STAT）家族成员相关。
Mol Cell Biol. 1994 May;14(5):3186-96. doi: 10.1128/mcb.14.5.3186-3196.1994.
10
Interleukin 6 promotes murine lupus in NZB/NZW F1 mice.白细胞介素6促进NZB/NZW F1小鼠的狼疮病情发展。
J Clin Invest. 1994 Aug;94(2):585-91. doi: 10.1172/JCI117373.

白细胞介素6激活热休克蛋白90β基因的表达。

Interleukin 6 activates heat-shock protein 90 beta gene expression.

作者信息

Stephanou A, Amin V, Isenberg D A, Akira S, Kishimoto T, Latchman D S

机构信息

Department of Molecular Pathology, University College London Medical School, U.K.

出版信息

Biochem J. 1997 Jan 1;321 ( Pt 1)(Pt 1):103-6. doi: 10.1042/bj3210103.

DOI:10.1042/bj3210103
PMID:9003407
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1218042/
Abstract

The levels of the cytokine interleukin-6 (IL-6) and the heat-shock protein hsp90 have both been reported to be elevated in patients with active systemic lupus erythematosus (SLE). We show that hsp90 protein accumulates to increased levels in both HuH7 hepatoma cells and peripheral blood mononuclear cells (PBMCs) treated with IL-6. In PBMCs this effect occurs without induction of the other hsps, paralleling the specific elevation of hsp90 in SLE. IL-6 is able to activate the hsp90 gene promoter directly; this activation can also be achieved by overexpressing either of the transcription factors NF-IL-6 or NF-IL-6 beta whose synthesis is induced by IL-6 treatment. Hence the induction of hsp90 protein accumulation by IL-6 is likely to be dependent on the enhanced activity of the hsp90 beta gene promoter produced by increased levels of NF-IL-6 and/or NF-IL-6 beta. These effects are discussed in terms of the role of hsp90 in the normal immune system and the mechanism of its activation in patients with SLE.

摘要

据报道，细胞因子白细胞介素-6（IL-6）和热休克蛋白hsp90的水平在活动性系统性红斑狼疮（SLE）患者中均升高。我们发现，在用IL-6处理的HuH7肝癌细胞和外周血单核细胞（PBMC）中，hsp90蛋白积累至升高水平。在PBMC中，这种效应在未诱导其他热休克蛋白的情况下发生，这与SLE中hsp90的特异性升高相似。IL-6能够直接激活hsp90基因启动子；通过过表达转录因子NF-IL-6或NF-IL-6β中的任何一种也可实现这种激活，它们的合成由IL-6处理诱导。因此，IL-6诱导hsp90蛋白积累可能依赖于NF-IL-6和/或NF-IL-6β水平升高所产生的hsp90β基因启动子活性增强。本文根据hsp90在正常免疫系统中的作用及其在SLE患者中的激活机制对这些效应进行了讨论。