| First Author | Granholm NA | Year | 1994 |
| Journal | Autoimmunity | Volume | 17 |
| Issue | 3 | Pages | 195-202 |
| PubMed ID | 7948604 | Mgi Jnum | J:19022 |
| Mgi Id | MGI:67235 | Doi | 10.3109/08916939409010654 |
| Citation | Granholm NA, et al. (1994) Pathogenesis of early nephritis in lupus prone mice with a genetic accelerating (lpr) factor. Autoimmunity 17(3):195-202 |
| abstractText | We investigated the relative roles of B cell activity, circulating immune complexes, complement concentration and kinetics of disappearance and uptake of immune complexes from the circulation in the pathogenesis of early nephritis of MRL/lpr mice. In comparison to data in control (C57BL/6J) mice, B cell activity was enhanced and the concentration of autoantibodies and endogenous immune complexes in plasma were increased, whereas complement (C3) concentration was not significantly different in MRL/lpr mice. The kinetics of disappearance of radiolabeled immune complexes from the circulation were similar in MRL/lpr and control mice, whereas uptake of radiolabeled immune complexes by the liver was decreased in MRL/lpr mice. Features of polyclonal B cell activation and impaired mononuclear phagocyte function are early events that may set the stage for progressive systemic involvement in MRL/lpr mice. |
