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 transplantations of highly nucleated, metabolically active solid organs, and it 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), such decrease of donor-specific HLA-antibodies is not uncommon after liver transplantation. While this phenomenon represents a metabolic achievement of the graft in overcoming one of the mechanism of rejection, respective observations on anti-A/B-isoagglutinins are missing, because these more aggressive antibodies have always to be removed before transplantation. <br>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.