In cardiac allografts, deposition of C4d in capillaries, accompanied by fibrin deposition, is predictive of graft loss and appears to be useful for the identification of patients with humoral rejection in need to modified immunosuppressive therapy. In renal allograft biopsies more than twelve months after transplantation, endothelial C4d deposition was found to be associated with contemporaneous or subsequent chronic transplant glomerulopathy, with basement membrane multilayering in peritubular capillaries and with an accumulation of mononuclear inflammatory cells (but not granulocytes) in peritubular capillaries 2. A second group of C4d-positive patients present with only mild allograft dysfunction and no histological signs of rejection: these patients patients did not show histological features suggestive of an antibody mediated type of rejection and do not appear to significantly benefit from antirejection therapy 1. Aggressive antirejection therapy in instances of C4d-positive acute cellular rejection episodes may be beneficial. In the early transplanted kidney, linear deposition of C4d occurs along peritubular capillaries in association with transplant glomerulitis: C4d deposition correlates with tubular MHC class II expression, panel-reactive antibody titers and raised serum creatinine levels at the time of biopsy. Studies have variously been performed on frozen sections by an indirect immunofluorescence technique 1 and on paraffin-embedded tissue 2. In addition, a humoral response to donor antigens is known to occur but is difficult to demonstrate in routine practice. Acute cellular rejection is identifiable on H/E sections. Immunohistochemical expressionÄendritic reticulum cells retain C4d: tonsil provides a useful control tissue.Ĭapillary endothelium in humoral rejection. Polyvalent antiserum against C4d allows staining in paraffin sections. The C4b is unstable, releasing C4c into the circulation and leaving bound C4d. Activated C1s cleaves C4 to release C4a into the circulation and C4b, which binds endothelium. It is generated via the classical antibody-induced pathway. C4d C4d C4d is a stable remnant of classical complement activation which becomes covalently bound to endothelium and basement membrane, rendering it persistent.
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