Abstract

Transplantation immunity is that branch of immunology that deals with the familiar destruction or rejection of grafts exchanged between genetically disparate individuals [I]. The successful employment of allografts, such as kidneys and hearts, for therapeutic replacement purposes currently requires ongoing treatment of the host with immunosuppressive drugs to hold in abeyance his immunological response against the alien cell surface histocompatibility antigens ofthe graft, especially those determined by the major histocompatibility complex (MHC). Tissue typing can reduce somewhat the magnitude of this histoincompatibility barrier, so that less immunosuppression is needed. The immune response that an allograft elicits in a normal or inadequately immunosuppressed host is the consequence of a complex interaction between the foreign antigens of the graft and various subsets of host lymphocytes and antigen-presenting cells (APC). The effectors generated during this host response, which mediate graft rejection, are various lymphocytes and antibodies, depending on the type of graft involved. Well before the science of immunogenetics emerged, allografts of both normal and malignant tissues were transplanted to heterotopic sites for different reasons [2]. These included technical convenience (as in the propagation of malignant tissues), confirmation of endocrine function, ability to observe grafts directly by transplanting to the anterior chamber of the eye or to the wall of the hamster's cheek pouch, and possibly the hope that they might serendipitously escape rejection altogether or at least thrive better than in other sites. The results obtained, together with the relatively high proportion of successes that has long been obtained with full- or partial-thickness therapeutic corneal allografts in nonimmunosuppressed patients, indicated that some sites do behave as if they

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