1994 Volume 36 Issue 4 Pages 322-330
To evaluate the role of cell-mediated immunity in acute poststreptococcal glomerulonephritis (APSGN), we identified the immune cell population infiltrating the glomeruli. Renal biopsies were obtained from 22 patients with APSGN, 16 with overt and 6 with asymptomatic disease, one to 30 days after onset. Samples of normal renal tissue were used as controls. Frozen sections were examined using monoclonal antibodies that recognize various leukocyte surface markers. Double staining for granulocytes and monocyte/macrophages (Mφ) was performed using chloroesterase staining and indirect immuno-alkalinephosphatase staining with Leu M-5 sequentially. In overt APSGN, there was a sub stantial increase in the total number of granulocytes and Mφ with a slight increase in T cells. Numbers correlated with time after onset, as more leukocytic infiltration was observed when the tissue was taken earlier. Furthermore, a significant positive linear correlation was seen between helper/inducer T cells and Mφ (r = 0.86, p < 0.01). Helper T cells tended to be increased to a higher proportion during the early stage, while suppressor T cells remained constant throughout the course. Analysis with anti proliferating cell nuclear antigen antibody revealed increased glomerular cell proliferation in the early phase of APSGN. In asymptomatic patients, the total number of leukocytes was less than in the overt patients, but the proportions of infiltrating cells were similar. These data suggest that Mφ are important effector cells causing endothelial and mesangial cell proliferation in APSGN. Mφ infiltration in the glomeruli appears to be mediated by complementinduced chemotaxis and probably be an antigen specific event related to the delayed type hypersensitivity mediated by helper/inducer T cells.
