Spontaneous and therapeutic glycosidic accommodation of host and graft in ABO(H)-incompatible transplantation, a hypothesis.

In contrast to non-nucleated ABO(H) 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; it is extremely rare in liver transplantations (Adams, 1991) (Della-Guardia et al., 2008) and does not occur in successful bone marrow engraftment (Takahashi, 2005). 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 (Bastani, 2006), and according to Taner et al. (2014)<i> </i>such transient decrease of donor-specific HLA-antibodies is not uncommon after incompatible liver transplantation. Treatment of pure red cell aplasia (PRCA) with ABO incompatible RBC, after ABO blood group incompatible hematopoietic stem cell transplantation, was followed by spontaneous decrease of isoagglutinin levels in several individuals (Stussi et al. 2009). In addition, an exponential fall in both anti-A/B reactive IgM and IgG titers was 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 pre-existing anti-graft-reactive immunoglobulins are adsorbed on complementary sites on the cell surfaces of the graft, but unlike on the surfaces of metabolically weak red cells, appear to be completed by graft-phenotype-specific protective glycosylation and may only recover when the graft-intrinsic enzymatic power and supply of specific substrates are exhausted.