The ABO blood group system is the most important blood type system (or blood group system) in human blood transfusion. The associated anti-A antibodies and anti-B antibodies are usually IgM antibodies, which are usually produced in the first years of life by sensitization to environmental substances such as food, bacteria and viruses. ABO blood types are also present in some animals, for example cows and sheep, and apes such as chimpanzees, bonobos, and gorillas.
The A antigen and the B antigen are derived from a common precursor known as the H antigen (or H substance). The H antigen is a carbohydrate sequence with carbohydrates linked mainly to protein (with a minor fraction attached to ceramide moiety). The majority of the ABO determinants are expressed on the ends of long polylactosamine chains attached mainly to Band 3 protein (1), the anion exchange protein of the red cell membrane, and a minority of the epitopes are expressed on neutral glycosphingolipids (1). In blood group O, the H antigen remains unchanged and consists of a chain of beta-D-galactose, beta-D-N-acetylglucosamine, beta-D-galactose, and 2-linked, alpha-L-fucose, the chain being attached to the protein or ceramide. H antigens can be changed into A or B antigens by enzymes coded by the blood group A or B genes, which are sugar (glycosyl) tranferases. Type A has an extra alpha-N-acetyl-D-galactosamine bonded to the D-galactose at the end, while type B has an extra alpha-D-galactose bonded to the D-galactose at the end.
One caveat to this axiom of 'universal donor' is that this applies to packed RBC's and not to whole blood products. Using the first table, type O carries anti-A and anti-B antibodies in the serum. To transfuse a type A, B, or AB recipient with type O whole blood would produce a hemolytic transfusion reaction due to the antibodies found in the serum of whole blood.
|A||A or O|
|B||B or O|
|AB||A, B, AB, or O|
Antibodies are not formed against the H antigen, except by those with the Bombay phenotype.
In ABH secretors, ABH antigens are secreted by most mucus-producing cells of the body interfacing with the environment, including lung, skin, liver, pancreas, stomach, intestines, ovaries and prostate.
Landsteiner described A, B, and O; Decastrello and Sturli discovered the fourth type, AB, in 1902. Ludwik Hirszfeld and E. von Dungern discovered the heritability of ABO blood groups in 1910–11, with Felix Bernstein demonstrating the correct blood group inheritance pattern of multiple alleles at one locus in 1924. . Watkins and Morgan, in England, discovered that the ABO epitopes were conferred by sugars, specifically N-acetylgalactosamine for the A-type and galactose for the B-type (Morgan, W. T. J. & Watkins, W. M. Br. Med. Bull. 25, 30–34 (1969), Watkins, W. M. in: Advances in Human Genetics Vol. 10 (eds Harris, H. & Hirschhorn, K.) 1–136 (Plenum, New York, 1980), Watkins, W. M. & Morgan, W. T. J. Vox Sang. 4, 97−119 (1959). After much published literature claiming that the ABH substances were all attached to glycosphingolipids, Laine's group (1988) found that the band 3 protein expressed a long polylactosamine chain (Jarnefelt, Rush, Li, Laine, J. Biol. Chem. 253: 8006–8009(1978)) which contained the major portion of the ABH substances attached (Laine and Rush in Molecular Immunology of Complex Carbohydrates (A. Wu, E. Kabat, Eds.) Plenum Publishing Corporation, N.Y. NY (1988)). Later, Yamamoto's group (Yamamoto, et al., Nature 345, 229–233 (1990)), showed the precise glycosyl transferase set that confers the A, B and O epitopes.
Anti-A and anti-B antibodies, which are not present in the newborn, appear in the first years of life. It is possible that food and environmental antigens (bacterial, viral or plant antigens) are similar enough to A and B glycoprotein antigens that antibodies created against the environmental antigens in the first years of life can cross react with ABO-incompatible red blood cells. Anti-A and anti-B antibodies are usually IgM, which are not able to pass through the placenta to the fetal blood circulation. O-type individuals can produce IgG-type ABO antibodies.
The "Light in the Dark theory" (DelNagro, 1998) suggests that when budding viruses take with them host cell membranes from one human patient (in particular from the lung and mucosal epithelium where they are highly expressed) they also take along ABO blood antigens from those membranes, and may carry them into secondary recipients where these antigens can elicit a host immune response against these non-self foreign blood antigens. These viral-carried human blood antigens may be responsible for priming newborns into producing neutralizing antibodies against foreign blood antigens. Support for this theory has come to light in recent experiments with HIV. HIV can be neutralized in "in-vitro" experiments using antibodies against blood group antigens specifically expressed on the HIV producing cell lines.
The "Light in the Dark theory" suggests a new novel evolutionary hypothesis that there is true communal immunity, which has developed to reduce the inter-transmissibility of viruses within a population. It suggests that individuals in a population supply and make a diversity of unique antigenic moieties so as to keep the population as a whole more resistant to infection. A system set up ideally to work with variable recessive alleles.
ABO blood group incompatibilities between the mother and child does not usually cause hemolytic disease of the newborn (HDN) because antibodies to the ABO blood groups are usually of the IgM type, which do not cross the placenta; however, in an O-type mother, IgG ABO antibodies are produced and the baby can develop ABO hemolytic disease of the newborn.
|Blood group inheritance|
|O||O||O, A||O, B||A, B|
|A||O, A||O, A||O, A, B, AB||A, B, AB|
|B||O, B||O, A, B, AB||O, B||A, B, AB|
|AB||A, B||A, B, AB||A, B, AB||A, B, AB|
Blood groups are inherited from both parents. The ABO blood type is controlled by a single gene with three alleles: i, IA, and IB. The gene encodes a glycosyltransferase—that is, an enzyme that modifies the carbohydrate content of the red blood cell antigens. The gene is located on the long arm of the ninth chromosome (9q34).
The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. Individuals with IAIA or IAi have type A blood, and individuals with IBIB or IBi have type B. IAIB people have both phenotypes, because A and B express a special dominance relationship: codominance, which means that type A and B parents can have an AB child. A type A and a type B couple can also have a type O child if they are both heterozygous (IBi,IAi) Therefore, an O child is not a direct proof of illegitimacy, just as a child with blond hair could be born from parents who both had brown hair. The cis-AB phenotype has a single enzyme that creates both A and B antigens. The resulting red blood cells do not usually express A or B antigen at the same level that would be expected on common group A1 or B red blood cells, which can help solve the problem of an apparently genetically impossible blood group.
In the UK, the distribution of blood type frequencies through the population still shows some correlation to the distribution of placenames and to the successive invasions and migrations including Vikings, Danes, Saxons, Celts, and Normans who contributed the morphemes to the placenames and the genes to the population.
There are six common alleles of the gene that produce one's blood type:A
Many rare variants of these alleles have been found in human populations around the world.
Some evolutionary biologists theorize that the IA allele evolved earliest, followed by O (by the deletion of a single nucleotide, shifting the reading frame) and then IB. This chronology accounts for the percentage of people worldwide with each blood type. It is consistent with the accepted patterns of early population movements and varying prevalent blood types in different parts of the world: for instance, B is very common in populations of Asian descent, but rare in ones of Western European descent.) Another theory states that there are four main lineages of the ABO gene and that mutations creating type O have occurred at least three times in humans. From oldest to youngest, these lineages comprise the following alleles: A101/A201/O09, B101, O02 and O01. The continued presence of the O alleles is hypothesized to be the result of balancing selection. Both theories, contradict the previously-held theory that type O blood evolved earliest, supported by the fact that all human beings can receive it. The British National Blood Transfusion Service states this to be the case (see the web-link under External Links below) and says that originally all human beings were type O.
The ABO antigen is also expressed on the von Willebrand factor (vWF) glycoprotein, which participates in hemostasis (control of bleeding). In fact, having type O blood predisposes to bleeding, as 30% of the total genetic variation observed in plasma vWF is explained by the effect of the ABO blood group, and individuals with group O blood normally have significantly lower plasma levels of vWF (and Factor VIII) than do non-O individuals. In addition, vWF is degraded more rapidly due to the higher prevalence of blood group O with the Cys1584 variant of vWF (an amino acid polymorphism in VWF): the gene for ADAMTS13 (vWF-cleaving protease) maps to the ninth chromosome (9q34), the same locus as ABO blood type. Higher levels of vWF are more common amongst people who have had ischaemic stroke (from blood clotting) for the first time. The results of this study found that the occurrence was not affected by ADAMTS13 polymorphism, and the only significant genetic factor was the person's blood group.
Individuals with the rare Bombay phenotype (hh) do not express substance H on their red blood cells, and therefore do not bind A or B antigens. Instead, they produce antibodies to substance H (which is present on all red cells except those of hh genotype) as well as to both A and B antigens, and can therefore receive blood only from other hh donors (although they can donate as though they were type O).
In parts of Europe the "O" in ABO blood type is substituted with "0" (zero), signifying the lack of A or B antigen. In the former USSR blood types are referenced using numbers and Roman numerals instead of letters. This is Janský's original classification of blood types. It designates the blood types of humans as I, II, III, and IV, which are elsewhere designated, respectively, as O, A, B, and AB. The designation A and B with reference to blood groups was proposed by Ludwik Hirszfeld.
In the slide testing method shown above, three drops of blood are placed on a glass slide with liquid reagents. Agglutination indicates the presence of blood group antigens in the blood.
In April 2007 an international team of researchers announced in the journal Nature Biotechnology an inexpensive and efficient way to convert types A, B and AB blood into type O. This is done by using glycosidase enzymes from specific bacteria to strip the blood group antigens from red blood cells. The removal of A and B antigens still does not address the problem of the Rhesus blood group antigen on the blood cells of Rhesus positive individuals, and so blood from Rhesus negative donors must be used. Patient trials will be conducted before the method can be relied on in live situations.
There are numerous popular myths surrounding ABO blood groups. These beliefs have existed since the ABO blood groups were identified and can be found in different cultures throughout the world. For example, during the 1930s, connecting blood groups to personality types became popular in Japan and other areas of the world.
The popularity of Peter J. D'Adamo's book, Eat Right For Your Blood Type suggests that these myths persist. This book claims that ABO blood groups can be used to determine diet as well as to predict diseases.
Additional myths include the idea that Group A causes severe hangovers, group O is associated with perfect teeth, and those with blood group A2 have the highest IQs. Scientific evidence in support of these concepts is scant or nonexistent.
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