Interleukin-1 and Interleukin-1 Receptor Antagonist in Systemic Lupus Erythematosus

Abstract

Interleukin-1 (IL-1) is thought to play an important role in the immunopathology of systemic lupus erythematosus (SLE). IL-1 receptor antagonist (IL-lra) exhibits a dose-responsive inhibition of IL-1 effects, and Fcr receptors play a key role in IL-lra production. To clarify the relationship between IL-1, IL-1 receptor antagonist (IL-lra) production, and Fcr receptors in SLE, fifteen untreated lupus patients (9 females and 6 males) were evaluated. IL-1 and IL-lra production from both monocytes and neutrophils was determined by both a murine thymocyte proliferation assay and ELISA. The expression of Fcr receptors on both monocytes and polymorphonuclear cells was measured by flow cytometry. There was no significant difference between IL-1 beta and IL-lra production from ex vivo monocytes between lupus patients and normals. However, serum IL-lra was significantly higher in lupus patients than in normals. The expression of FcrRII (CD32) on monocytes was lower in lupus patients than in normals. There was no correlation between the expression of FcrRII and the serum immune complexes; the production of IL-lra and the expression of CD32, serum immune complex levels, and serum IgG. Both serum IL-ra and the production of IL-lra had no correlation to SLEDAI, C3, C4, Clq, or ESR. These observations suggest that although IL-1 and IL-lra may not play a major role in the initiation of pathogenesis of lupus, the low FcrRII expression in lupus may reflect low immune complex clearance and contribute to disease pathogenesis.