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Updated: Aug 18, 2026

An Efficient Sieving Method to Isolate Intact Glomeruli from Adult Rat Kidney
Published on: November 1, 2018
Cell-mediated immune response in acute poststreptococcal glomerulonephritis
N Yoshizawa1, T Oda, Y Oshikawa
1Second Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Abstract:
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 (M phi) was performed using chloro-esterase staining and indirect immuno-alkaline-phosphatase staining with Leu M-5 sequentially. In overt APSGN, there was a substantial increase in the total number of granulocytes and M phi 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 M phi (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 M phi are important effector cells causing endothelial and mesangial cell proliferation in APSGN. M phi infiltration in the glomeruli appears to be mediated by complement-induced chemotaxis and probably be an antigen-specific event related to the delayed type hypersensitivity mediated by helper/inducer T cells.
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