Role of fibrinogen-like protein 2 prothrombinase/fibroleukin in experimental and human allograft rejection.

摘要: Immune coagulation is a major contributor to the pathogenesis of xenograft rejection, viral-induced hepatocellular injury and cytokine-induced fetal loss syndrome. In this study, we investigated contribution novel gene product, fibrinogen-like protein 2 (fgl2) prothrombinase, in mediating immune experimental human acute allograft rejection. Using mouse heterotopic cardiac transplant model, fgl2 (mfgl2)/fibroleukin mRNA transcripts were highly expressed macrophages, CD4- CD8-positive T lymphocytes, endothelial cells rejecting allografts association with deposits fibrin. Although mfgl2-deficient mice rejected at similar rates littermate controls, survival grafts from prolonged deposition intravascular fibrin was diminished. Treatment wild-type neutralizing anti-fgl2 Ab ameliorated histological evidence for allorejection deposition, resulted an increase graft survival. To address further relevance examined kidney biopsies patients who had undergone renal transplantation. Human markedly mainly tubule cells, infiltrating lymphoid including CD8 + mature B (plasma cells), cells. Dual staining showed localized blood vessels, glomerulus interstitium lumen tubules, occurred expression. These data collectively suggest that accounts seen both rejection provide rationale targeting as adjunctive therapy treat