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.

与输注至HLA相合的O(H)血型受者后数分钟内即发生破坏的无核ABO(H)不相容红细胞不同，这类超急性体液排斥反应（hyperacute, humoral rejection）在高有核、代谢活跃的实体器官移植中相对少见，在肝移植中更是极为罕见（Adams等，1991；Della-Guardia等，2008）。此外，Bastiani（2006）曾报道1例HLA不相容肝移植术后预先存在的供者特异性HLA抗体（donor-specific HLA-antibodies）选择性消失的病例；而Taner等（2014）指出，肝移植术后供者特异性HLA抗体水平下降并非罕见现象。尽管这类现象被视为移植物在克服某一排斥反应机制过程中的代谢适应性表现，但目前尚无针对抗A/B同种凝集素（anti-A/B-isoagglutinins）的相关观察研究，因为这类攻击性更强的抗体通常需在移植术前予以清除。
现有研究表明，移植器官始终保留其原有的表型（phenotype）特异性代谢特性；拓展糖基化排除（glycosidic exclusion）概念可知，表型可同时调控细胞表面与免疫球蛋白的糖基化修饰。因此可推测，ABO不相容且代谢活跃的移植组织，可借助其表型特异性酶系统，通过持续糖基化修饰HLA相合受者血浆蛋白与B细胞表面的互补位点，从而构建相容的体内环境。