Abstract
The aim of this study was to create a model of antibody mediated rejection (AMR) to allow studies into the pathogenesis and treatment of AMR in the absence of cellular rejection which is generally well controlled by current therapies. Sprague Dawley (SD) rats were immunized with Wistar spleen cells and 7 days later (day 0) underwent bilateral nephrectomy and received an orthotopic Wistar renal allograft. Recipient rats were killed 4 days later. Following induction of the alloantibody response, recipient rats underwent T cell depletion by administration of OX-19 antibody beginning 3 days before transplantation. Flow cytometric analysis of blood cells and immunostaining of allografts and spleen tissue confirmed T cell depletion. High titres of donor specific antibodies were detected in serum by flow cytometry using Wistar thymocytes, while immunostaining showed prominent endothelial deposition of IgG and C4d in renal allografts. Allograft dysfunction was evident on day 4 with elevated serum creatinine and histological damage featuring glomerulopathy, peritubular capillaritis, acute tubular damage, leukocytic infiltrates and thrombosis. Immunostaining identified platelet deposition and infiltrates of macrophages, neutrophils and NK cells in allografts. In conclusion, we have developed a rat model which mimics the main features of acute AMR and is suitable for therapeutic studies.
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