Journal
JOURNAL OF IMMUNOLOGY
Volume 184, Issue 9, Pages 4605-4609Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903595
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Funding
- National Institutes of Health [RO1 AI42269, RO1 AI 49954, K23 AR055672]
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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-23-R 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-23-R mediated signaling in the development of lupus nephritis and urge the consideration of proper biologics for the treatment of the disease. The Journal of Immunology, 2010, 184: 4605-4609.
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