alexa Cutting edge: IL-23 receptor deficiency prevents the development of lupus nephritis in C57BL 6-lpr lpr mice.
Immunology

Immunology

Rheumatology: Current Research

Author(s): Kyttaris VC, Zhang Z, Kuchroo VK, Oukka M, Tsokos GC

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Abstract 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.
This article was published in J Immunol and referenced in Rheumatology: Current Research

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