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.
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