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Updated: May 9, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Treatment with anti-interleukin 23 antibody ameliorates disease in lupus-prone mice
Vasileios C Kyttaris1, Ourania Kampagianni, George C Tsokos
1Division of Rheumatology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, CLS-936, Boston, MA 02215, USA. vkyttari@bidmc.harvard.edu
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.

