T lymphocyte subsets in systemic lupus erythematosus. Correlations with corticosteroid therapy and disease activity.
The contribution of immune regulation to the etiology of systemic lupus erythematosus (SLE) is poorly understood. Using the monoclonal antibodies OKT4 and OKT8, we quantitated, by flow cytometry, T inducer/helper and T cytotoxic/suppressor cells in patients with SLE. Serologically active patients, who had clinical manifestations such as arthritis or rash and were not receiving prednisone, were characteristically lymphopenic due to a marked reduction in OKT4+ cells. Prednisone therapy produced the same phenomenon. Untreated patients, who were serologically inactive, demonstrated no abnormalities. These studies have thus revealed two presumably independent factors that can produce similar immunoregulatory aberrations.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000328:Adult; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000145:classification* / Q000276:immunology
D000305:Adrenal Cortex Hormones