Defective production of interleukin 1 and interleukin 2 in patients with systemic lupus erythematosus (SLE).

Mariana Linker‐Israeli(University of Southern California), A C Bakke(University of Southern California), Rodanthi C. Kitridou(University of Southern California), Sandra Gendler(University of Southern California), Steven Gillis(University of Southern California), David A. Horwitz(University of Southern California)
The Journal of Immunology
June 1, 1983
Cited by 450

Abstract

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.


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