Pathogenesis of early nephritis in lupus prone mice with a genetic accelerating (lpr) factor.

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.