How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to an HLA-compatible blood group O(H) recipient undergo destruction within minutes, such hyperacute, humoral rejection occurs relatively rare in HLA-incompatible transplantations of highly nucleated, metabolically active solid organs, and is extremely rare in liver transplantations (Adams 1991; Della-Guardia et al. 2008;). Moreover, a case of selective disappearance of preexisting donor-specific HLA-antibodies after HLA-incompatible liver transplantation has been reported by Bastiani (2006), and according to Taner et al. (2014), decreased donor-specific antibody levels are not uncommon after liver transplantation. While this phenomenon represents a metabolic achievement of the graft, respective observations on anti-A/B-isoagglutinins are missing, because these more aggressive antibodies are always removed before transplantation. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.