Cutting Edge: IL-23 Receptor Deficiency Prevents the Development of Lupus Nephritis in C57BL/6–lpr/lpr Mice | Zendy

Vasileios C. Kyttaris | Zendy; Zheng Zhang | Zendy; Vijay K. Kuchroo | Zendy; Mohamed Oukka | Zendy; George C. Tsokos | Zendy

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Cutting Edge: IL-23 Receptor Deficiency Prevents the Development of Lupus Nephritis in C57BL/6–lpr/lpr Mice

Author(s) -

Vasileios C. Kyttaris,

Zheng Zhang,

Vijay K. Kuchroo,

Mohamed Oukka,

George C. Tsokos

Publication year - 2010

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.0903595

Subject(s) - lupus nephritis , systemic lupus erythematosus , medicine , immunology , cd8 , adoptive cell transfer , lymph , lymph node , cd3 , disease , pathology , immune system , t cell

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.

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