IL-17–producing T cells infiltrate kidneys of patients with lupus nephritis, and IL-23–treated lymph node cells from lupus-prone mice may transfer disease to Rag1-deficient mice. In this study, we show that IL-23R–deficient lupus-prone C57BL/6–lpr/lpr mice display decreased numbers of CD3+ CD4− CD8− cells and IL-17A–producing cells in the lymph nodes and produce less anti-DNA Abs. In addition, clinical and pathology measures of lupus nephritis are abrogated. The presented experiments document the importance of IL-23R–mediated signaling in the development of lupus nephritis and urge the consideration of proper biologics for the treatment of the disease.