Carpenter J P, Tomaszewski J E
Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, USA.
J Vasc Surg. 1998 Mar;27(3):492-9. doi: 10.1016/s0741-5214(98)70323-4.
Although it has been claimed that allografts of blood vessels might be successful because of minimal immunogenicity, they are subject to frequent and early failure, the cause of which has not been thoroughly investigated. We sought to define the immune response to allograft bypass. In a prospective trial, 40 patients underwent cryopreserved venous allograft bypass. Allograft biopsies were performed at implantation and at allograft explantation in instances of graft failure. Tissues were evaluated in a blinded manner by means of standard histologic examination and paraffin immunohistochemical analysis with monoclonal antibodies against a variety of immune markers. During the 31-month follow-up period, 22 allografts were removed, and 19 were suitable for immunohistochemical study. Of these 19, 6 (32%) had moderate or severe infiltrates, which were evenly distributed throughout the intima, media, and adventitia. Immunohistochemical study of the explants demonstrated all of these infiltrates to be leukocytes (+LCA), which were predominantly activated T lymphocytes (+CD3, CD8, CR3) containing cytotoxic granules (+TIA-1). Macrophages were uncommon (+CD68); B cells (+L26, CD79) and natural killer cells (+CD56) were rare. Immunosuppression was associated with decreased presence of cytotoxic granules (TIA-1). Human venous 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 possible to modify the contribution of rejection to venous allograft failure by means of immunosuppression and to modify the contribution of local hypercoagulability by means of anticoagulation.
