Physiological and therapeutic glycosidic adaptation of host to graft or graft to host in ABO(H)-incompatible transplantation, a hypothesis.

In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to a 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 transient, selective disappearance of preexisting donor-specific HLA-antibodies after an incompatible liver transplantation, without any rejection episodes, has been reported by Bastiani (2006), and according to Taner et al. (2014), such transient decrease of donor-specific HLA-antibodies is not uncommon after liver transplantation. In addition, a transient exponential fall in both anti-A/B reactive IgM and IgG titers were also observed after ABO(H) incompatible bone marrow transplantation (Rowley et al. 2000; Lee et al. 2003). These phenomena most likely reflect a complex mechanism, in which the simple adsorption of the host immunoglobulins by graft epitopes is completed by graft-phenotype-specific glycosylation of these immunoglobulins. 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 A/B metabolically active, solid tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of the non-completed, free H-receptor sites of the plasma proteins and the differentiating B-cell surfaces of an O(H) recipient.