HUMAN SAPHENOUS-VEIN ALLOGRAFT BYPASS GRAFTS - IMMUNE-RESPONSE

Although it has been claimed that allografts of blood vessels might be successful because of minimal immunogenicity, they are subject to fre quent and early failure, the cause of which has not been thoroughly in vestigated. We sought to define the immune response to allograft bypas s. In a prospective trial, 40 patients underwent cryopreserved venous allograft bypass. Allograft biopsies were performed at implantation an d at allograft explantation in instances of graft failure. Tissues wer e evaluated in a blinded manner by means of standard histologic examin ation and paraffin immunohistochemical analysis with monoclonal antibo dies against a variety of immune markers. During the 31-month follow-u p period, 22 allografts were removed, and 19 were suitable for immunoh istochemical study. Of these 19, 6 (32%) had moderate or severe infilt rates, which were evenly distributed throughout the intima, media, and adventitia. Immunohistochemical study of the explants demonstrated al l of these infiltrates to be leukocytes (+LCA), which were predominant ly activated T lymphocytes (+CD3, CD8, CR3) containing cytotoxic granu les (+TIA-1). Macrophages were uncommon (+CD68); B cells (+L26, CD79) and natural killer cells (+CD56) were rare. Immunosuppression was asso ciated with decreased presence of cytotoxic granules (TIA-1). Human ve nous allografts are immunogenic and prompt a T cell-mediated response. Allografts also fail without strong evidence of rejection, presumably because of local injury, hypercoagulability, or stasis. It may be pos sible to modify the contribution of rejection to venous allograft fail ure by means of immunosuppression and to modify the contribution of lo cal hypercoagulability by means of anticoagulation.