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- W2117127436 abstract "Abstract . It has been reported previously that one-third of protocol renal biopsies in asymptomatic, biochemically stable renal transplant recipients in the first 6 mo show unsuspected subclinical graft rejection (both infiltrate and tubulitis) and that subclinical rejection is a risk factor for chronic renal dysfunction. This study was performed to determine whether differences in phenotype or activation status of graft-infiltrating cells underlie these different manifestations of acute rejection. Biopsies with normal histology ( n = 10), subclinical rejection ( n = 13), and clinical rejection ( n = 9) were studied using immunohistochemistry and computerized image analysis. Subclinical and clinical rejections had similar histologic Banff scores. Univariate analysis showed a trend for a higher infiltration with CD8+ ( P = 0.053) and CD68+ ( P = 0.06) cells in clinical rejection. Of the activation markers studied (CD25, perforin, tumor necrosis factor-α), only allograft inflammatory factor-1 +-activated macrophages were significantly ( P = 0.014) increased in the infiltrate of clinical rejection biopsies. These data suggest that activated macrophages or their products are responsible for acute renal dysfunction associated with clinical rejection episodes." @default.
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- W2117127436 date "1999-07-01" @default.
- W2117127436 modified "2023-10-10" @default.
- W2117127436 title "Clinical Rejection Is Distinguished from Subclinical Rejection by Increased Infiltration by a Population of Activated Macrophages" @default.
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- W2117127436 doi "https://doi.org/10.1681/asn.v1071582" @default.
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