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Immunological response against allogeneic chondrocytes transplanted into joint surface defects in rats
Institution:1. From the Department of Endocrinology, St. Vincent’s Hospital, Sydney, New South Wales, Australia;2. University of Sydney, Sydney, New South Wales, Australia;3. SydPath, St. Vincent’s Hospital, Sydney, New South Wales, Australia;4. St. Vincent’s Clinical School, University of New South Wales, Sydney, New South Wales, Australia;5. Diabetes and Metabolism, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.;1. NanoBioCel Group, Laboratory of Pharmacy and Pharmaceutical Technology, University of the Basque Country, Paseo de la Universidad 7, UPV/EHU, Vitoria-Gasteiz, Spain;2. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine, CIBER-BBN, Vitoria-Gasteiz, Spain;3. University College of London UCL Institute for Liver and Digestive Health, Royal Free Hospital Campus, Rowland Hill street, Hampstead, UCL Medical School, London NW3 2PF, UK;4. University College of London UCL Division of Surgery and Interventional Science, Royal Free Hospital Campus, Pond St, Hampstead, UCL Medical School, London NW3 2QG, UK
Abstract:Rat chondrocytes isolated from the articular-epiphyseal cartilage complex were transplanted into defects prepared in articular cartilage and subchondral bone. Transplants were taken for examination after 3 and 8 wk. Cartilage formed by syngeneic chondrocytes did not evoke formation of infiltrations. Contrary to that, in the vicinity of cartilage produced by allogeneic chondrocytes numerous infiltrating cells were present and cartilage resorption could be observed. Cyclosporine-A (CsA) treatment of recipients of allogeneic chondrocytes only partially suppressed accumulation of infiltrating cells and matrix resorption. Antichondrocyte immune response of chondrocyte graft recipients was studied by evaluation of spleen mononuclear cells (SMC) stimulation in mixed splenocytechondrocyte cultures and by evaluation of antichondrocyte cytotoxic antibodies. No difference in stimulation of SMC from intact rats by syngeneic and allogeneic chondrocytes was observed. Stimulation by allogeneic chondrocytes was slightly but significantly higher in recipients of syngeneic grafts. SMC of allogenic chondrocyte recipients were strongly stimulated by allogeneic chondrocytes. This response was absent in recipients treated with CsA. Spontaneous antichondrocyte cytotoxic antibody activity was detected in intact rats and in recipients of syngeneic grafts. In recipients of allogeneic chondrocytes the antibody response against allogeneic chondrocytes was raised but was statistically not significant owing to the considerable variation in the level of spontaneously occurring antichondrocyte antibodies.
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