Anderson J L, Greenwood J H, Kawanishi H
Br Heart J. 1981 Oct;46(4):410-4. doi: 10.1136/hrt.46.4.410.
Several diseases with autoimmune features have recently been shown to be characterised by defects in suppressor cell immune regulation. Aberrant immune mechanisms of primary importance have been sought but not yet demonstrated for idiopathic congestive cardiomyopathy and rheumatic heart disease. We tested whether defective immunoregulatory function might explain certain features of these diseases. Peripheral blood mononuclear cells from patients with both diseases showed normal proliferative responses in the mixed leucocyte reaction. Concanavalin A induced similar suppressor activity, quantified in mixed leucocyte reaction as a suppression index, among control subjects, patients with rheumatic heart disease, and patients with idiopathic congestive cardiomyopathy. Similarly, patient serum supported induction of suppressor activity in normal leucocytes equal to that of control serum. A chronic immunoregulatory defect thus does not appear necessary for the development of idiopathic congestive cardiomyopathy or rheumatic heart disease.
最近有研究表明，几种具有自身免疫特征的疾病的特点是抑制性细胞免疫调节存在缺陷。人们一直在寻找特发性充血性心肌病和风湿性心脏病的首要异常免疫机制，但尚未得到证实。我们测试了免疫调节功能缺陷是否可以解释这些疾病的某些特征。这两种疾病患者的外周血单个核细胞在混合淋巴细胞反应中显示出正常的增殖反应。在对照受试者、风湿性心脏病患者和特发性充血性心肌病患者中，伴刀豆球蛋白A诱导的抑制活性在混合淋巴细胞反应中以抑制指数进行量化，结果相似。同样，患者血清对正常白细胞中抑制活性的诱导作用与对照血清相当。因此，特发性充血性心肌病或风湿性心脏病的发生似乎并不需要慢性免疫调节缺陷。
