Central immunological position of the human histo (blood) group O(H).

2017-06-22T14:20:34Z (GMT) by Peter Arend
<p>Prokaryotic "blood group A/B-like" antigenic structures basically induce cross-reactive anti-A/B immunoglobulins, which due to clonal selection neither arise in blood group A nor in B individuals but occur predominantly or exclusively in blood group O. While bacterial endotoxins non-specifically stimulate the formation of all immunoglobulins, involving the anti-A/B isoagglutinins, a definite, adaptive immunological induction of these agglutinins appears to be restricted to blood group O(H) individuals. In the non-O blood groups, anti-A/B reactivity is exerted by a primarily polyreactive, thymus-independent non-immune IgM molecule that has undergone the phenotype-specific, glycosidic accommodation of plasma proteins, which reduces or excludes anti-self reactivity and even explains the survival of highly nucleated ABO incompatible transplants, however, necessarily involves impairment of immunity. While blood group A phenotype development thus is associated with impaired formation of adaptive and innate immunoglobulins, it promotes susceptibility to malaria infection via its intrinsic enzyme functions, initiating a self-destructive glycosidic, phenotypic accommodation of a "wrong eukaryote". Indeed, blood group A phenotype-specific GalNAc transferase activities, expressed by both cell surfaces and plasma proteins, and serine/threonine kinases from <i>Plasmodium falciparum</i>, which over the parasite's life cycle get into the red blood cell (RBC) of the human host, might provide the metabolic condition for adhesion protein and RBC rosette formation, assumingly based on heterologous <i>O</i>-glycosylation, breaking a species barrier and completing the "serine repeat antigen". Thus, the obvious protection of human blood group O(H) individuals from severe malaria infection may be explained by the lack of blood group A phenotype-specific GalNAc glycosylation(s), and suggests a new molecular definition of the immunological (therapeutic) target. In fact, the human histo (blood) group O finally represents the worldwide most common blood type, associated with a superior complex immunity, which in the non-O blood groups is reduced through phenotypic, identical glycosylation of cell surfaces and plasma proteins.</p><p> </p><p> </p><p></p><p></p><p></p><p></p><p></p>