Immune facilitation of allograft survival across restricted differences at the H-2 complex.

Abstract

Numerous studies have now documented that a number of parallels exist between the overt immune response of lower and higher vertebrates to allografts.1,2 In both, the immune response is influenced by a number of factors the most prominent of which are the genetic disparity between the donor and host and the type of tissue employed as an allograft. Whether across weak or strong histocompatibility barriers, skin grafts elicit the most vigorous response. This is manifested as chronic rejection across weak barriers and acute rejection across major barriers. Heart and kidney grafts, however, elicit a varied response.3,4,5 In the urodels,6 and certain semi-inbred strains of fish,7 heart grafts persist indefinitely or are rejected over a long time course. In inbred strains of rats3,4,5 and mice,8,9 kidney and in some instances, whole heart grafts are either rejected as rapidly as skin grafts or exhibit a prolonged survival time. In each group of animals, a correlation has been found between the strength of the genetic incompatibility and the duration of graft survival.10 A similar correlation has been found between the immunogenetic strength of histocompatibility antigens and the capacity of alloantibody to enhance graft survival.11 That is, it has been shown that it is easier to enhance the survival of grafts across weak barriers than strong barriers.