(Redirected from Type O blood)
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,
apes such as
chimpanzees,
bonobos and
gorillas.
ABO antigens
Diagram showing the carbohydrate chains which determine the ABO blood group
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
glycosphingolipid (
sphingolipid with
carbohydrates linked to the
ceramide moiety). Since it lacks N-acetylneuraminic acid (
sialic acid) it is referred to as a
globoside, not a ganglioside. In blood group O the H antigen remains unchanged and consists of a chain of
galactose,
N-Acetylglucosamine, galactose, and
fucose attached to the ceramide. H antigens can be changed into A or B antigens by
enzymes coded by the blood group A or B genes. Type A has an extra
N-Acetylgalactosamine bonded to the galactose near the end, while type B has an extra galactose bonded to the galactose near the end.
Individuals with Type A blood can accept blood from donors of type A and type O blood. Individuals with type B blood can receive blood from donors of type B and type O blood. Individuals with type AB blood may receive blood from donors of type A, type B, type AB, or type O blood. Type AB blood is referred to as the universal recipient. Individuals of type O blood may receive blood from donors of type O blood. Type O blood is called the universal donor.
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.
History of discoveries
The ABO blood group system is widely credited to have been discovered by the Austrian scientist
Karl Landsteiner, who found three different blood types in 1900;
[ Zur Kenntnis der antifermentativen, lytischen und agglutinierenden Wirkungen des Blutserums und der Lymphe, Landsteiner K, , , Zentralblatt Bakteriologie, 1900 ] he was awarded the
Nobel Prize in Physiology or Medicine in 1930 for his work. Due to inadequate communication at the time it was subsequently found that Czech serologist
Jan Janský had independently pioneered the classification of human blood into four groups,
[ (Haematologick studie u. psychotiku, Janský J, , , Sborn. Klinick, 1907 ] but Landsteiner's independent discovery had been accepted by the scientific world while Janský remained in relative obscurity. Janský's classification is however still used in Russia and states of former USSR (see below). In America Moss published his own (very similar) work in 1910.
[ Studies on isoagglutinins and isohemolysins, Moss WL, , , Bulletin Johns Hopkins Hospital, 1910 ]
Landsteiner described A, B, and O; Decastrello and Sturli discovered the fourth type, AB, in 1902.
[ Ueber die Isoagglutinine im Serum gesunder und kranker Menschen, von Decastello A, Sturli A, , , Mfinch med Wschr, 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.
[1]
Serology
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.
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.
[2]
[3]
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 hemolytic disease of the newborn
Main articles: ABO hemolytic disease of the newborn
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, sometimes
IgG ABO antibodies are produced and a baby can develop
ABO hemolytic disease of the newborn.
Inheritance
| 'Blood group inheritance' |
| Mother/Father | 'O' | 'A' | 'B' | 'AB' |
|---|---|---|---|---|
| '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'', ''I
A'', and ''I
B''. 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).
''I
A'' allele gives type A, ''I
B'' gives type B, and ''i'' gives type O. ''I
A'' and ''I
B'' are dominant over ''i'', so ''ii'' people have type O, ''I
AI
A'' or ''I
Ai'' have A, and ''I
BI
B'' or ''I
Bi'' have type B. ''I
AI
B'' 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 (I
Bi,I
Ai) Therefore, an O child is not a direct proof of illegitimacy. 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 A
1 or B red blood cells, which can help solve the problem of an apparently genetically impossible blood group.
[ The cis-AB blood group phenotype: fundamental lessons in glycobiology, Yazer M, Olsson M, Palcic M, , , Transfus Med Rev, 2006 ]
Some evolutionary biologists theorize that the ''I
A'' allele evolved earliest, followed by ''O'' (by the deletion of a single nucleotide, shifting the
reading frame) and then ''I
B''. 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.) This, however, contradicts the more commonly stated 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.
Population data
The distribution of the blood groups A, B, O and AB varies across the world according to the population. There are also variations in blood type distribution within human subpopulations.
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.
[ English Medieval Settlement, , WTW, Potts, St. Martin's Press, 1979, ISBN 0-7131-6257-0 ]
Association with von Wilebrand factor
The ABO antigen is also expressed on the
von Willebrand factor (vWF)
glycoprotein,
[4] which participates in
hemostasis (control of bleeding). In fact, having type O blood predisposes to bleeding,
[5] as 30% of the total genetic variation observed in plasma vWF is explained by the effect of the ABO blood group,
[6] and individuals with group O blood normally have significantly lower plasma levels of vWF (and
Factor VIII) than do non-O individuals.
[7][8] 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):
[9] 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.
[10] 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.
Bombay phenotype
Main articles: Hh antigen system
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 are therefore compatible only with other ''hh'' donors.
Nomenclature in Europe and former USSR
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.
[ Blood Group Classifications, a Plea for Uniformity, Erb IH, , , Canadian Medical Association Journal, 1940 ] The designation A and B with reference to blood groups was proposed by
Ludwik Hirszfeld.
Examples of ABO and Rhesus D slide testing method
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.
Universal blood created from other types
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.
[11] 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.
Artificial Blood
Researchers at Sheffield University announced in May 2007, they have developed an artificial plastic blood which could act as a substitute in emergencies
BBC.
References
1. Felix Bernstein and the first human marker locus, Crow J, , , Genetics, 1993
2.
Antibody to histo-blood group A antigen neutralizes HIV produced by lymphocytes from blood group A donors but not from blood group B or O donors., , M, Arendrup, AIDS,
3.
HIV-1 incorporates ABO histo-blood group antigens that sensitize virions to complement-mediated inactivation, , SJ, Neil, Blood,
4. Role of A and B blood group antigens in the expression of adhesive activity of von Willebrand factor, , R, Sarode, Br J Haematol.,
5. The relationship between ABO histo-blood group, factor VIII and von Willebrand factor, , J, O'Donnell, Transfus Med.,
6. Amount of H antigen expressed on circulating von Willebrand factor is modifiedby ABO blood group genotype and is a major determinant of plasma von Willebrand factor antigen levels, , J, O'Donnell, Arterioscler Thromb Vasc Biol.,
7. The effect of ABO blood group on the diagnosis of von Willebrand disease, , JC, Gill, Blood,
8. ABO blood group genotype and plasma von Willebrand factor in normal individuals, , M, Shima, Vox Sang,
9. The prevalence of the cysteine1584 variant of von Willebrand factor is increased in type 1 von Willebrand disease: co-segregation with increased susceptibility to ADAMTS13 proteolysis but not clinical phenotype, , DJ, Bowen, Br J Haematol,
10. High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability., Bongers T, de Maat M, van Goor M, et. al, , , Stroke, 2006
11. Bacterial glycosidases for the production of universal red blood cells, , QP, Liu, Nat Biotechnol, 2007
Further reading
★
Chapter 5: The ABO blood group. Dean L
★
Blood group serology--the first four decades (1900--1939), Farr A, , , Med Hist, 1979
External links
★
ABO at BGMUT Blood Group Antigen Gene Mutation Database at
NCBI,
NIH
★
Blood Grouping techniques
★
Encyclopaedia Britannica, ABO blood group system
★
National Blood Transfusion Service
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