GENERAL CLINICAL RESEARCH CENTER

大量研究表明系统性红斑狼疮（SLE）的病因 是多因素的，尽管大多数研究表明， 系统是自身免疫性疾病表达的最终途径。 一些 一系列证据已经发现细胞介导的免疫缺陷和特异性免疫缺陷。 T-抑制细胞的缺陷已被证实。 家族研究， 特别是双胞胎研究，已经显示出免疫状态改变的高发生率， 家庭成员中SLE的发病率增加， 单卵双胞胎SLE发病率超过50%。 其他研究表明 环境影响与淋巴细胞毒性抗体的存在， SLE家庭成员以及密切的家庭接触者。 如果免疫学 异常可以在SLE家族成员中表现出来，特别是 抑制性T细胞缺陷，这一点，与存在的 抗淋巴细胞抗体，将支持SLE表现为 在那些有遗传倾向的人身上， 环境刺激 本提案的目的是证明 这样的缺陷。 该研究计划将选择50名系统性红斑狼疮患者家属和1名对照 一组50名年龄、种族和性别匹配的非家庭密切接触者。 所有 受试者将接受SLE血清学异常筛查， 进行迟发型超敏反应皮肤试验。 淋巴细胞毒性抗体将 在所有组中进行测试，并鉴定任何T细胞功能 畸变 在研究的最后阶段，那些T细胞 已经确定的异常将有一个深入的研究T 抑制-辅助细胞缺陷。

Numerous studies have shown the etiology of Systemic Lupus Erythematosus (SLE) to be multifactorial though most investigations have shown an altered immune system to be the final pathway in expression of the autoimmune disease. Some lines of evidence have found a defect in cell mediated immunity and a specific defect of T-suppressor cells has been demonstrated. Familial studies, especially twin studies, have shown a high incidence of altered immune status in family members, an increased incidence of SLE among family members and a greater than 50% incidence of SLE among monozygotic twins. Other studies have suggested an environmental influence with the presence of lymphocytotoxic antibodies in SLE family members as well as close household contacts. If immunologic abnormalities can be demonstrated in SLE family members, specifically a suppressor T cell defect, this, in conjunction with the presence of anti-lymphocyte antibodies, would support the hypothesis that SLE manifests itself in those persons with a genetic predisposition given the appropriate environmental stimulus. It is the objective of this proposal to demonstrate such a defect. The research plan will select 50 family members of SLE patients and a control group of 50 non-family close contacts matched for age, race, and sex. All subjects will be screened for serologic abnormalities seen in SLE and have delayed hypersensitivity skin tests performed. Lymphocytotoxic antibodies will be tested for in all groups and identification of any T cell function aberration. In the final phase of the study, those subjects in whom T cell abnormalities have been identified will have an in-depth study of T suppressor-helper cell defects.