How an ABO-incompatible graft may be protected 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 an 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. In addition, an 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 represent a transient metabolic achievement of the graft in overcoming rejection. 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.