| First Author | Kyttaris VC | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 9 | Pages | 4605-9 |
| PubMed ID | 20308633 | Mgi Jnum | J:160486 |
| Mgi Id | MGI:4454515 | Doi | 10.4049/jimmunol.0903595 |
| Citation | Kyttaris VC, et al. (2010) Cutting edge: IL-23 receptor deficiency prevents the development of lupus nephritis in C57BL/6-lpr/lpr mice. J Immunol 184(9):4605-9 |
| abstractText | 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. |
