Abstract

Interleukin 23 receptor expressing IL-17 producing T cells have been shown to be important in the development of murine lupus. The usefulness of IL-23 inhibition in ameliorating lupus nephritis is unknown. We hypothesized that inhibition of IL-23 will ameliorate nephritis in lupus-prone mice. To this end, we treated MRL/lpr lupus-prone mice for 6 weeks with a rat anti-IL-23p19 antibody, which resulted in delaying the onset of nephritis without affecting the production of anti-dsDNA antibodies. The effect of the treatment was hampered by the production of murine anti-rat IgG antibodies. The amelioration of murine lupus by IL-23 inhibition strengthens the rationale for targeting IL-23 in patients with systemic lupus erythematosus.

Highlights

  • Interleukin 23 (IL-23) is a member of the IL-12 family that is important for the generation and maintenance of Th17 cells

  • Several lines of evidence suggest that Th17 cells may play an important role in Systemic lupus erythematosus (SLE) and in particular lupus nephritis; for example, SLE T cells produce IL-17 spontaneously while IL-17+ T cells are found in the kidneys of SLE patients with nephritis

  • We have previously shown that lupus-prone mice (B6/lpr) that are genetically deficient in the receptor for IL-23 were protected from the massive lymphoproliferation, production of pathogenic anti-dsDNA antibodies, and the development of nephritis [5]

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Summary

Introduction

Interleukin 23 (IL-23) is a member of the IL-12 family that is important for the generation and maintenance of Th17 cells. We have previously shown that lupus-prone mice (B6/lpr) that are genetically deficient in the receptor for IL-23 were protected from the massive lymphoproliferation, production of pathogenic anti-dsDNA antibodies, and the development of nephritis [5]. We provide evidence that treatment of lupus-prone mice with antiIL-23 antibodies ameliorates nephritis through inhibition of the production of IL-17 by T cells.

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