Immune mechanisms and molecular mediators of glomerular injury in experimental nephritis. Summary of current results and continuing studies.

Despite a growing body of evidence on the importance of macrophage accumulation in renal glomeruli to the subsequent injury in experimental immune nephritis, exact mechanisms of the monocyte/macrophage recruitment and phenomena leading to tissue damage are not completely clarified. Our experiments indicate that neutral proteinases released in situ by activated macrophages may, at least in part, be responsible for the development of autoimmune nephrotoxic glomerulonephritis in rats. Accordingly, apart from the well-established features of glomerular hypercellularity and basement membrane damage, a new mechanism of direct cytolysis by macrophage-derived proteinases is postulated to be of potential relevance to the nephritic glomerular injury.