Central immunological position of the human histo (blood) group O(H).
Peter Arend
10.6084/m9.figshare.4714618.v146
https://figshare.com/articles/journal_contribution/Central_immunological_position_of_the_human_histo_blood_group_O_H_/4714618
<p>Prokaryotic
"blood group A/B-like" antigenic structures basically induce
cross-reactive anti-A/B immunoglobulins, which neither
arise in blood group A nor in B individuals due to clonal selection 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>
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2017-07-16 22:04:03
Aberrant expression
Cancer