How an ABO-incompatible graft may be protected by phenotypespecific 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 a HLA-incompatible liver transplantation without any rejection episodes, 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 they are always removed before transplantation. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO(H)-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 differentiating B-cell surfaces of a HLA-compatible recipient.