Histo (blood) group A2 phenotype and "irregular"anti-A1-reactive IgM arise in identical glycosylation

The phenotypes of the human ABO(H) histo (blood) group) system and its non-immune isoagglutinin specificities arise in a process, which was termed "glycosidic exclusion", and represents a physiological principle, through which (in normal conditions) the simultaneous appearance of a phenotype and its corresponding innate (auto) antibody is reduced or excluded by identical glycosylations of complementary domains on cell surfaces, secretions and plasma proteins that involve the neonatal non-immune IgM molecule. Because the different blood group A subtypes are predominantly determined by genetically different GalNAc transferring proteins or functions, the developmental isolation of the so-called "irregular" anti-A₁ reactivity in some plasmas of blood group A₂ individuals most likely results from the lack of GalNAc transferase A₁ and exclusive encoding of a specific GalNAc transferase A₂.