Natvig J B, Harboe M, Fausa O, Tveit A
Clin Exp Immunol. 1971 Feb;8(2):229-36.
The immunoglobulins were studied in twenty-one individuals with isolated lack of γA-globulin and in eleven of their families. The propositi were normal blood donors and patients with ataxia telangiectasia, with rheumatoid arthritis, or in a few cases other conditions. With the exception of one family where the mother and one child lacked γA, no family members other than the propositi were affected. In the family members, the levels of γA-globulin and of other immunoglobulins were mostly within normal ranges. Furthermore, there was no association between the lack of γA-globulin and the Gm marker system. Anti-γA antibodies were found in seven propositi. The findings demonstrated that the lack of γA-globulin was usually not due to structural gene defects, but indicated some regulatory mechanism, with depression of γA synthesis.
对21例单纯缺乏γA球蛋白的个体及其11个家族的免疫球蛋白进行了研究。先证者为正常献血者以及患有共济失调毛细血管扩张症、类风湿性关节炎的患者,少数情况下为患有其他疾病的患者。除了一个家庭中母亲和一个孩子缺乏γA外,除先证者外没有其他家庭成员受到影响。在家庭成员中,γA球蛋白和其他免疫球蛋白的水平大多在正常范围内。此外,γA球蛋白缺乏与Gm标记系统之间没有关联。在7例先证者中发现了抗γA抗体。研究结果表明,γA球蛋白缺乏通常不是由于结构基因缺陷,而是提示存在某种调节机制,导致γA合成受到抑制。