Mechanisms of chronic renal allograft rejection. II. Progressive allograft glomerulopathy in miniature swine.

摘要: We have reported that in thymectomized miniature swine treated with a 12-day course of cyclosporin A major histocompatibility complex class I-mismatched renal allografts either progress to chronic rejection (progression group; n = 4) or tolerance after acute (recovery 4). Two types glomerulopathies, termed and allograft glomerulopathy, occur this model. Morphological immunohistochemical studies were performed on serial biopsies from both groups examine the pathogenic mechanisms glomerulopathy. In rejection, glomerulopathy developed by Day 18, antibody deposition T cell macrophage infiltration. situ DNA nick end-labeling (TUNEL)+ injured glomerular endothelial cells appeared early phase, followed destruction capillary network segmental mesangiolysis. Thereafter, progression group, progressed during development rejection. This process was associated persistent infiltration, deposition, TUNEL+ injury glomeruli. Impaired repair, mesangial proliferation, activation still noted at 100, together accumulation matrix duplication basement membrane. contrast, recovery recovered resolution cellular infiltration reduction deposition. conclude cell- antibody-mediated against is key determinant toward repair phenotypic change also contribute With tolerance, substantial can inflammation.