前沿：IL-23 受体缺陷可预防 C57BL/6-lpr/lpr 小鼠狼疮肾炎的发生。
Cutting edge: IL-23 receptor deficiency prevents the development of lupus nephritis in C57BL/6-lpr/lpr mice.
机构信息
Division of Rheumatology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, CLS-937, Boston, MA 02215, USA.
出版信息
J Immunol. 2010 May 1;184(9):4605-9. doi: 10.4049/jimmunol.0903595. Epub 2010 Mar 22.
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.
摘要
IL-17 产生 T 细胞浸润狼疮肾炎患者的肾脏，并且来自狼疮易感小鼠的 IL-23 处理的淋巴结细胞可能将疾病转移到 Rag1 缺陷型小鼠。在这项研究中，我们表明 IL-23R 缺陷型狼疮易感 C57BL/6-lpr/lpr 小鼠在淋巴结中显示出减少的 CD3(+)CD4(-)CD8(-)细胞和产生 IL-17A 的细胞的数量，并且产生更少的抗 DNA Abs。此外，狼疮肾炎的临床和病理学措施被消除。所呈现的实验证明了 IL-23R 介导的信号在狼疮肾炎发展中的重要性，并敦促考虑适当的生物制剂来治疗该疾病。
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