类风湿关节炎家族中淋巴细胞O6-甲基鸟嘌呤修复缺陷可能是一种后天性缺陷。
Deficient repair of O6-methylguanine in lymphocytes from rheumatoid arthritis families may be an acquired defect.
作者信息
Colaço C B, Harris G, Lawley P D, Lydyard P M, Roitt I M
机构信息
Department of Immunology, Middlesex Hospital Medical School, London, UK.
出版信息
Clin Exp Immunol. 1988 Apr;72(1):15-9.
Deficient repair of the premutagenic DNA lesion O6-methylguanine (O6-MeGua) has been reported in lymphocytes from patients with autoimmune diseases. This was confirmed in the present study of probands with rheumatoid arthritis (RA) and their families. We also noted a significant deficiency in 9/19 spouses (P less than 0.05) and a statistically non-significant deficiency of repair of O6-MeGua in 14/42 first and second degree relatives in comparison with healthy and non-autoimmune disease controls, respectively. A significant correlation of the repair status of O6-MeGua in DNA between individual probands with RA and respective spouses (P less than 0.01) and probands and respective family members (P less than 0.001) supported the idea that an environmental, transmissible agent could influence the expression of the protein, O6-methylguanine-DNA-transferase (O6-MT), involved in the repair of O6-MeGua. The present results, however, cannot entirely exclude an additional hereditary influence.
据报道，自身免疫性疾病患者淋巴细胞中诱变前DNA损伤O6-甲基鸟嘌呤（O6-MeGua）的修复存在缺陷。这在本项针对类风湿性关节炎（RA）先证者及其家族的研究中得到了证实。我们还注意到，与健康对照和非自身免疫性疾病对照相比，19名配偶中有9名存在显著缺陷（P<0.05），42名一级和二级亲属中有14名O6-MeGua修复存在统计学上不显著的缺陷。类风湿性关节炎个体先证者与其各自配偶（P<0.01）以及先证者与各自家庭成员（P<0.001）之间DNA中O6-MeGua修复状态的显著相关性支持了这样一种观点，即一种环境可传播因子可能会影响参与O6-MeGua修复的蛋白质O6-甲基鸟嘌呤-DNA转移酶（O6-MT）的表达。然而，目前的结果不能完全排除额外的遗传影响。
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