Modulation of Ia and leukocyte common antigen expression in rat glomeruli during the course of glomerulonephritis and aminonucleoside nephrosis.

We have investigated changes in the glomerular expression of two antigens, Ia and leukocyte common (LC) antigens, during the course of two models of glomerular injury in the rat. Acute glomerulonephritis induced by nephrotoxic, antiglomerular basement membrane antiserum is accompanied by a 3-fold increase in the number of glomerular cells expressing Ia and LC antigens. Acquisition of the Ia+ phenotype appears to occur in LC+ monocytes that have assumed subendothelial and intramesangial positions. Enhanced Ia expression is seen over a wide range of proteinuria. Decomplementation prior to nephrotoxic, antiglomerular basement membrane anti-serum administration abrogates both the proteinuria and the increased Ia expression; an increase in cells expressing LC antigen still occurs. The chronic phase of nephrotoxic, antiglomerular basement membrane antiserum-induced glomerulonephritis is associated with a persistent increase in glomerular Ia+ cells residing primarily in the mesangium. In the glomerulopathy induced by the aminonucleoside of puromycin, there are two phases of glomerular Ia modulation. In the first week, there is a decrease in Ia expression by LC+ cells. The second week is marked by infiltration by monocytes and an increase in Ia expression by both resident and infiltrating cells. Modulation of the Ia phenotype on resident and infiltrating marrow-derived cells carries implications with respect to the immunologic pathogenesis of both models of glomerular injury.