Miller K B, Schwartz R S
N Engl J Med. 1979 Oct 11;301(15):803-9. doi: 10.1056/NEJM197910113011502.
We tested the hypothesis that abnormalities of central immune function are genetically controlled in patients with systemic lupus erythematosus. We used an in vitro suppressor-cell assay to evaluate central immunoregulation in 15 patients, 50 of their clinically healthy family members and 41 normal persons. Impaired suppressor-cell function was found in 11 patients; there was no correlation between disease activity and test results. Abnormal suppressor-cell activity was also found in 13 first-degree relatives, 12 of whom were women. We found no correlation between results of the suppressor-cell assay and the presence or absence of lymphocytotoxic antibodies in the relatives. Impaired suppressor-cell function cannot by itself explain the pathogenesis of systemic lupus erythematosus. Our results support the hypothesis that certain abnormalities of suppressor cells are genetic markers. We propose that the development of systemic lupus erythematosus requires the participation of at least two functionally distinct classes of genes.
系统性红斑狼疮患者的中枢免疫功能异常受基因控制。我们采用体外抑制细胞试验对15例患者、其50名临床健康的家庭成员及41名正常人的中枢免疫调节功能进行了评估。11例患者存在抑制细胞功能受损;疾病活动度与检测结果之间无相关性。在13名一级亲属中也发现了异常的抑制细胞活性,其中12名是女性。我们发现抑制细胞试验结果与亲属中淋巴细胞毒性抗体的有无之间无相关性。抑制细胞功能受损本身并不能解释系统性红斑狼疮的发病机制。我们的结果支持如下假设:抑制细胞的某些异常是基因标记。我们提出,系统性红斑狼疮的发病需要至少两类功能不同的基因参与。