| First Author | Kitching AR | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 1 | Pages | 1-10 |
| PubMed ID | 9933080 | Mgi Jnum | J:52913 |
| Mgi Id | MGI:1330655 | Doi | 10.1002/(SICI)1521-4141(199901)29:01<1::AID-IMMU1>3.0.CO;2-R |
| Citation | Kitching AR, et al. (1999) IL-12 directs severe renal injury, crescent formation and Th1 responses in murine glomerulonephritis. Eur J Immunol 29(1):1-10 |
| abstractText | Glomerular crescent formation characterizes severe glomerulonephritis (GN). Evidence suggests that crescent formation results from a delayed-type hypersensitivity-like Th1 response. As IL-12 directs Th1 responses, we tested the hypothesis that IL-12 is important in crescentic GN. Neutralization of IL-12 attenuated crescent formation and cell-mediated injury in C57BL/6 mice sensitized to and challenged with sheep anti-mouse glomerular basement membrane (GBM) globulin. Recombinant IL-12 induced severe crescentic GN with enhanced Th1 responses in C57BL/6 mice in which non-crescentic GN was induced by injecting anti-GBM globulin into naive mice. BALB/c mice do not develop significant crescent formation in these models, due either to regulatory effects of IL-4, or to deficits in IL-12 production/responsiveness. Administering IL-12 to BALB/c mice with GN induced Th1 responses and crescent formation, whereas IL-4-deficient BALB/c mice did not develop cell-mediated crescentic injury when GN was induced in sensitized mice. These results establish a central role for IL-12 in severe crescentic GN. |
