Defective production of interleukin 1 and interleukin 2 in patients with systemic lupus erythematosus (SLE).
The objective of this study was to define some causes of the immunologic impairment characteristic of systemic lupus erythematosus. Blood mononuclear cells from 19 patients were stimulated to produce interleukin 1 and interleukin 2 and compared with controls. A severe defect in both IL 1 and IL 2 activity was observed. The low cytokine levels did not correlate with clinical or serologic activity of disease. These defects could not be explained by concurrent corticosteroid therapy. There was no correlation between a lower number of OKT4+ cells observed in these patients and the levels of IL 2 production, nor did removal of monocytes bring IL 2 to normal. Impaired IL 2 production could not be restored to normal by IL 1. The observed deficiency in these regulatory cytokines may therefore be a primary defect that is important in the pathogenesis of this disorder.
D000818:Animals; D002448:Cell Adhesion; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000502:physiology; D007376:Interleukin-2 / Q000096:biosynthesis*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D009000:Monocytes / Q000276:immunology; D051381:Rats; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D007375:Interleukin-1; D007376:Interleukin-2; D013755:Tetradecanoylphorbol Acetate