GENERAL CLINICAL RESEARCH CENTER

大量研究表明系统性红斑狼疮(SLE)的病因 尽管大多数研究表明免疫力的改变是多因素的 系统是自身免疫性疾病表达的最终途径。一些人 一系列证据发现了细胞免疫的缺陷和一种特殊的 T抑制细胞的缺陷已被证实。家族研究， 尤其是双胞胎研究表明，在中国，免疫状态改变的发生率很高 家庭成员中系统性红斑狼疮的发病率增加， 同卵双胞胎中SLE的发病率超过50%。其他研究表明 淋巴细胞毒抗体的存在对环境的影响 SLE家庭成员以及密切的家庭接触者。如果免疫学 在SLE家族成员中可以表现出异常，特别是 抑制性T细胞缺陷，这与存在 抗淋巴细胞抗体，将支持SLE表现为 在那些具有遗传易感性的人身上给予适当的 环境刺激。这项提议的目的是证明 这样的缺陷。 该研究计划将选择50名SLE患者的家属和一名对照 由50名非家庭密切接触者组成的小组，年龄、种族和性别匹配。全 受试者将接受系统性红斑狼疮的血清学异常筛查，并 进行了迟发性超敏反应皮肤试验。淋巴毒素抗体会 在所有人群中进行测试，并确定任何T细胞功能 像差。在研究的最后阶段，研究对象中的T细胞 已发现异常情况将对T细胞进行深入研究 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.