90kda热休克蛋白在系统性红斑狼疮特定亚群中的升高。

V. Dhillon, S. McCALLUM, D. Latchman, D. Isenberg
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引用次数: 16

摘要

我们之前的研究表明,90 kDa热休克蛋白(hsp90)在伴有活动性神经精神(NP)和/或心肺(CR)疾病的狼疮患者中显著升高。这种升高依赖于hsp90 β基因转录的增强。一系列研究表明,hsp90水平的变化对NP、CR、血液学和肾性SLE的活性变化具有高度敏感性。我们现在提供的证据表明,狼疮患者中hsp90的过表达与抗磷脂综合征的存在有关,并且与在这一特定队列患者中最常见的HLA等位/单倍型的缺乏有关。我们认为,hsp90在SLE中的表达上调具有遗传基础,这可能直接参与了SLE患者亚群的发病机制。
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Elevation of the 90 kDa heat-shock protein in specific subsets of systemic lupus erythematosus.
We have previously shown that the 90 kDa heat-shock protein (hsp90) is notably elevated in lupus patients with active neuro-psychiatric (NP) and/or cardio-respiratory (CR) disease. This elevation is dependent upon enhanced transcription of the hsp90 beta gene. Serial studies have shown that changes in hsp90 levels have a high level of sensitivity for changes in activity of NP, CR, haematological and renal SLE. We now present evidence that overexpression of hsp90 in lupus patients is associated with the presence of the anti-phospholipid syndrome, and with the absence of the HLA allo-/haplotypes most commonly found in this particular cohort of patients. We conclude that the upregulation of hsp90 expression in SLE has a genetic basis, and that this may be directly involved in pathogenesis in subsets of patients with this disease.
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