The protein on the erythrocyte cell surface contain a wide selection of different oligosaccharides that are attached in a variety of ways to the proteins. However, it spite of the variation, there are a few structures that are extremely common. Among the most typical “core” constructions is something called H-antigen. It really is made up of many different sugars but the outside end of the H-antigen framework always consists of a fucose (Fuc) residue, a galactose residue (Gal), and an N-acetylglucosamine (GlcNAc) residue.

14) residues to create a branched framework by the end of the oligosaccharide (see diagram below). The enzyme that catalyzes this response is called N-acetylaminogalactosyltransferase or enzyme. The gene for this enzyme is situated on chromosome 9. The OMIN (Online Mendelian Inheritance in Man) access for the ABO blood group is 110300. Wealth is included by it of information on the topic. Normal red blood cells are recognized as “self”, so we don’t have antibodies against our own cells. However, we will have antibodies against the red bloodstream cells of other people’s bloodstream if their cell-surface sugars will vary from ours.

This is the basis of the ABO blood group and it’s why we have to match blood types in a bloodstream transfusion. The ABO blood group was found out over a hundred years ago by Karl Landsteiner (Nobel Laureate: Karl Landsteiner). The biochemical basis was only elucidated in the 1970’s when the technology for evaluating the carbohydrate structure of glycoproteins was worked out. There’s an allele of the A enzyme gene that involves only an extremely small number of mutations, but the result is to change the enzyme from one which exchanges GalNAc to one that exchanges galactose (Gal). The variant enzyme is named B-enzyme (galactosyltransferase) and the B antigen framework has a terminal galactose (Gal) instead of a terminal GalNAc.

If you are homozygous for the B allele on chromosome 9 then all your red bloodstream cells will have the B antigen oligosaccharide on their surface. You won’t make antibodies against this framework because it’s “self.” Additionally you learned have antibodies against H-antigen for the reason explained earlier. But you won’t recognize A antigen as self which means that your antibodies will attack any foreign cells which come from people with the normal wild-type allele (A). People with bloodstream type A will have antibodies against the B antigen.

They can obtain blood from people who have O bloodstream type however they will reject blood from people who have B blood type. You now have all the information you need to figure out who can give and receive blood from every possible mixture of alleles: AA, AO, AB, BO, and OO.

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There are no known natural effects of these differing blood types. People who have A, B, AB, and O phenotypes do not differ in fitness in any major way that we have had the opportunity to identify. This shows that the complete lack of the enzyme (null mutation) is natural in today’s human population and so is the change in one form of the enzyme to some other.

Suggestions that blood type determines susceptibility for some infections are normal in the technological literature. Many of them have not held up. The best relationship is a possible association between blood type susceptibility and O to cholera. The ABO alleles appear to be segregating in the human population by random genetic drift. The O allele (non-functional enzyme) is the most common allele. The B allele is minimal common-probably since it arose more recently.

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