Satoh H, Yokota E, Tokiyama K, Kawaguchi T, Niho Y
First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Ann Rheum Dis. 1991 Nov;50(11):765-8. doi: 10.1136/ard.50.11.765.
Sixty six patients with systemic lupus erythematosus (SLE) were genotyped using a HindIII restriction fragment length polymorphism identified by CR1.1 cDNA, then were followed up for an average of 50 months to evaluate the stability of their CR1 activities. The gene frequencies for the two alleles which correlate with the numeric expression of CR1 on the erythrocytes were not significantly different between 66 patients with SLE and 52 normal controls. A discrepancy between homozygosity for a high allele and a negative CR1 activity was found in many patients. These patients, however, had significantly lower concentrations of serum complement than did patients with a positive CR1, and some were in an active state of the disease. Furthermore, there were several patients in whom the CR1 activities changed from negative to positive together with an increase in serum complement. Our results suggest that the decreased expression of CR1 on erythrocytes in patients with SLE is not inherited, rather it is a consequence of the disease processes.
采用由CR1.1 cDNA鉴定的HindIII限制性片段长度多态性方法,对66例系统性红斑狼疮(SLE)患者进行基因分型,然后平均随访50个月,以评估其CR1活性的稳定性。与红细胞上CR1数值表达相关的两个等位基因的基因频率,在66例SLE患者和52例正常对照之间无显著差异。许多患者中发现高等位基因纯合性与CR1活性阴性之间存在差异。然而,这些患者的血清补体浓度显著低于CR1阳性的患者,且部分患者处于疾病活动状态。此外,有几名患者的CR1活性从阴性转变为阳性,同时血清补体增加。我们的结果表明,SLE患者红细胞上CR1表达降低并非遗传所致,而是疾病过程的结果。