Idiopathic membranous glomerulonephropathy (MG) has a rather benign prognosis. Acute renal failure with cellular crescents superimposed on MG is unusual and its pathogenesis is not fully understood. We report 3 patients with crescentic MG who showed strong glomerular and interstitial infiltration of leukocytes (CD45), T lymphocytes (CD3), helper/inducer T cells (CD4), cytotoxic/suppressor T cells (CD8), and monocyte-macrophages (CD14). A similar number of CD4+ and CD8+ cells contributed to T cellularity within the glomerular tuft, whereas CD4+ cells were predominant over CD8+ cells in the crescents. Intercellular adhesion molecule-1 (ICAM-1) antigens (CD54) were found on renal vascular endothelium, interstitial cellular aggregates and proximal tubular epithelial cells. The case reports illustrate the contribution of macrophages and T cells bearing predominantly CD4+ phenotype to cellular crescents, and the abnormal expression of ICAM-1 antigens on proximal tubular epithelial cells. Both features suggest that cell-mediated immunity may play a role in the transformation of crescentic MG.
Mesenchymal stem cells (MSC) have been shown to be immunomodulatory, tissue regenerative, and graft promoting; however, several questions remain with regard to ideal MSC source and timing of administration. In this study, we utilized a rigorous preclinical model of allogeneic islet cell transplantation, incorporating reduced immune suppression and near to complete mismatch of major histocompatibility antigens between the diabetic cynomolgus monkey recipient and the islet donor, to evaluate both the graft promoting impact of MSC source, that is, derived from the islet recipient, the islet donor or an unrelated third party as well as the impact of timing. Co-transplant of MSC and islets on post-operative day 0, followed by additional IV MSC infusions in the first posttransplant month, resulted in prolongation of rejection free and overall islet survival and superior metabolic control for animals treated with recipient as compared to donor or third-party MSC. Immunological analyses demonstrated that infusion of MSC from either source did not prevent alloantibody formation to the islet or MSC donor; however, treatment with recipient MSC resulted in significant downregulation of memory T cells, decreased antidonor T cell proliferation, and a trend toward increased Tregulatory:Tconventional ratios.
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