Dhillon V B, McCallum S, Latchman D S, Isenberg D A
Department of Molecular Pathology, University College Medical School, London, UK.
Q J Med. 1994 Apr;87(4):215-22.
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.
我们之前已经表明，90 kDa热休克蛋白（hsp90）在患有活动性神经精神（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hsp90β基因转录的增强。系列研究表明，hsp90水平的变化对NP、CR、血液学和肾脏SLE活动度的变化具有高度敏感性。我们现在提供证据表明，狼疮患者中hsp90的过表达与抗磷脂综合征的存在相关，并且与该特定患者群体中最常见的HLA等位基因/单倍型的缺失相关。我们得出结论，SLE中hsp90表达的上调具有遗传基础，并且这可能直接参与该疾病部分患者的发病机制。
