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Codomina Blood Type Reading for Elementary Students

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Classification of blood types

"Type O" redirects here. Not to be confused with Typo or Type 0.

The ABO blood grouping system is used to announce the presence of ane, both, or neither of the A and B antigens on erythrocytes.[1] For homo claret transfusions, it is the almost important of the 43 different blood blazon (or group) classification systems currently recognized past the International Society of Blood Transfusions (ISBT) as of June 2021.[2] [3] A mismatch (very rare in modern medicine) in this, or any other serotype, can cause a potentially fatal adverse reaction later a transfusion, or an unwanted immune response to an organ transplant.[4] The associated anti-A and anti-B antibodies are usually IgM antibodies, produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses.

The ABO blood types were discovered by Karl Landsteiner in 1901; he received the Nobel Prize in Physiology or Medicine in 1930 for this discovery.[5] ABO blood types are also present in other primates such every bit apes and Old World monkeys.[6]

History [edit]

Discovery [edit]

The ABO blood types were first discovered by an Austrian Physician Karl Landsteiner working at the Pathological-Anatomical Establish of the University of Vienna (at present Medical University of Vienna). In 1900, he found that red blood cells would clump together (agglutinate) when mixed in test tubes with sera from different persons, and that some human blood also agglutinated with animal blood.[7] He wrote a two-sentence footnote:

The serum of good for you human beings not just agglutinates animal crimson cells, but besides often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the issue of some harm of bacterial kind.[eight]

This was the first evidence that blood variations exist in humans – information technology was believed that all humans have similar blood. The next yr, in 1901, he made a definitive ascertainment that blood serum of an individual would agglutinate with but those of certain individuals. Based on this he classified human blood into 3 groups, namely group A, group B, and grouping C. He divers that group A blood agglutinates with group B, merely never with its ain type. Similarly, grouping B blood agglutinates with group A. Grouping C blood is different in that it agglutinates with both A and B.[9]

This was the discovery of claret groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. In his paper, he referred to the specific claret group interactions as isoagglutination, and likewise introduced the concept of agglutinins (antibodies), which is the actual basis of antigen-antibiotic reaction in the ABO organisation.[10] He asserted:

[It] may be said that at that place exist at least two different types of agglutinins, 1 in A, another one in B, and both together in C. The cherry-red blood cells are inert to the agglutinins which are present in the same serum.[nine]

Thus, he discovered two antigens (agglutinogens A and B) and ii antibodies (agglutinins - anti-A and anti-B). His 3rd group (C) indicated absence of both A and B antigens, just contains anti-A and anti-B.[10] The post-obit year, his students Adriano Sturli and Alfred von Decastello discovered the fourth blazon (but not naming information technology, and simply referred to it every bit "no particular blazon").[11] [12]

Ukraine marine uniform imprint, showing the wearer's blood type as "B (Iii) Rh+".

In 1910, Ludwik Hirszfeld and Emil Freiherr von Dungern introduced the term O (goose egg) for the grouping Landsteiner designated as C, and AB for the type discovered by Sturli and von Decastello. They were also the first to explain the genetic inheritance of the blood groups.[13] [14]

Nomenclature systems [edit]

Jan Janský, who invented blazon I, Ii, 3, 4 system.

Czech serologist Jan Janský independently introduced blood type classification in 1907 in a local journal.[15] He used the Roman numerical I, II, III, and Iv (corresponding to mod O, A, B, and AB). Unknown to Janský, an American md William L. Moss devised a slightly different classification using the same numerical;[16] his I, II, 3, and Iv corresponding to modernistic AB, A, B, and O.[12]

These two systems created defoliation and potential danger in medical practise. Moss's arrangement was adopted in Britain, France, and US, while Janský's was preferred in most European countries and some parts of US. To resolve the chaos, the American Clan of Immunologists, the Society of American Bacteriologists, and the Association of Pathologists and Bacteriologists fabricated a joint recommendation in 1921 that the Jansky classification be adopted based on priority.[17] Only information technology was not followed particularly where Moss's arrangement had been used.[18]

In 1927, Landsteiner had moved to the Rockefeller Institute for Medical Enquiry in New York. As a member of a commission of the National Enquiry Quango concerned with claret grouping, he suggested to substitute Janský's and Moss's systems with the letters O, A, B, and AB. (There was another confusion on the apply of effigy 0 for German language nothing as introduced by Hirszfeld and von Dungern, because others used the letter O for ohne, pregnant without or zero; Landsteiner chose the latter.[18]) This nomenclature was adopted by the National Inquiry Council and became variously known as the National Research Council nomenclature, the International nomenclature, and most popularly the "new" Landsteiner classification. The new system was gradually accustomed and by the early 1950s, it was universally followed.[19]

Other developments [edit]

The first practical use of blood typing in transfusion was past an American physician Reuben Ottenberg in 1907. And the big-calibration awarding started during the Showtime World War (1914-1915) when citric acid was developed equally blood clot prevention.[x] Felix Bernstein demonstrated the right blood group inheritance pattern of multiple alleles at i locus in 1924.[twenty] Watkins and Morgan, in England, discovered that the ABO epitopes were conferred by sugars, to be specific, N-acetylgalactosamine for the A-type and galactose for the B-blazon.[21] [22] [23] After much published literature claiming that the ABH substances were all attached to glycosphingolipids, Finne et al. (1978) found that the human erythrocyte glycoproteins contain polylactosamine chains[24] that contains ABH substances attached and correspond the majority of the antigens.[25] [26] [27] The main glycoproteins conveying the ABH antigens were identified to be the Band 3 and Band 4.5 proteins and glycophorin.[28] Afterwards, Yamamoto's group showed the precise glycosyl transferase set that confers the A, B and O epitopes.[29]

  • Diagram showing the carbohydrate chains that determine the ABO blood group

  • Student blood test. Three drops of claret are mixed with anti-B (left) and anti-A (right) serum.

  • There are three basic variants of immunoglobulin antigens in humans that share a very similar chemic structure but are distinctly dissimilar. Cerise circles show where there are differences in chemical construction in the antigen-binding site (sometimes called the antibody-combining site) of human being immunoglobulin. Notice the O-type antigen does not have a binding site.[thirty]

Genetics [edit]

Blood groups are inherited from both parents. The ABO claret type is controlled by a single cistron (the ABO factor) with 3 types of alleles inferred from classical genetics: i, IA , and IB . The I designation stands for isoagglutinogen, some other term for antigen.[31] The gene encodes a glycosyltransferase—that is, an enzyme that modifies the saccharide content of the red blood prison cell antigens. The factor is located on the long arm of the ninth chromosome (9q34).[ citation needed ]

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 take type O blood. Individuals with IAIA or IAi accept type A blood, and individuals with IBIB or IBi have type B. IAIB people take both phenotypes, because A and B limited a special authorisation relationship: codominance, which means that type A and B parents tin accept an AB kid. A couple with type A and type B can also have a type O child if they are both heterozygous (IBi,IAi). The cis-AB phenotype has a single enzyme that creates both A and B antigens. The resulting cherry-red blood cells do non usually express A or B antigen at the aforementioned level that would be expected on mutual group A1 or B red blood cells, which tin can assist solve the problem of an apparently genetically impossible blood grouping.[32]

Blood group inheritance
Claret type O A B AB
Genotype ii (OO) IAi (AO) IAIA (AA) IBi (BO) IBIB (BB) IAIB (AB)
O ii (OO) O
OO OO OO OO 		O or A
AO OO AO OO 		A
AO AO AO AO 		O or B
BO OO BO OO 		B
BO BO BO BO 		A or B
AO BO AO BO
A IAi (AO) O or A
AO AO OO OO 		O or A
AA AO AO OO 		A
AA AA AO AO 		O, A, B or AB
AB AO BO OO 		B or AB
AB AB BO BO 		A, B or AB
AA AB AO BO
IAIA (AA) A
AO AO AO AO 		A
AA AO AA AO 		A
AA AA AA AA 		A or AB
AB AO AB AO 		AB
AB AB AB AB 		A or AB
AA AB AA AB
B IBi (BO) O or B
BO BO OO OO 		O, A, B or AB
AB BO AO OO 		A or AB
AB AB AO AO 		O or B
BB BO BO OO 		B
BB BB BO BO 		A, B or AB
AB BB AO BO
IBIB (BB) B
BO BO BO BO 		B or AB
AB BO AB BO 		AB
AB AB AB AB 		B
BB BO BB BO 		B
BB BB BB BB 		B or AB
AB BB AB BB
AB IAIB (AB) A or B
AO AO BO BO 		A, B or AB
AA AO AB BO 		A or AB
AA AA AB AB 		A, B or AB
AB AO BB BO 		B or AB
AB AB BB BB 		A, B, or AB
AA AB AB BB

The table above summarizes the various claret groups that children may inherit from their parents.[33] [34] Genotypes are shown in the 2d column and in pocket-sized print for the offspring: AO and AA both examination every bit type A; BO and BB exam as blazon B. The 4 possibilities represent the combinations obtained when one allele is taken from each parent; each has a 25% run a risk, just some occur more than than once. The text above them summarizes the outcomes.

Claret grouping inheritance past phenotype simply
Blood type O A B AB
O O O or A O or B A or B
A O or A O or A O, A, B or AB A, B or AB
B O or B O, A, B or AB O or B A, B or AB
AB A or B A, B or AB A, B or AB A, B or AB

Historically, ABO blood tests were used in paternity testing, but in 1957 only 50% of American men falsely accused were able to use them as prove against paternity.[35] Occasionally, the claret types of children are non consistent with expectations—for example, a type O child can be built-in to an AB parent—due to rare situations, such as Bombay phenotype and cis AB.[36]

Subgroups [edit]

The A claret type contains about xx subgroups, of which A1 and A2 are the most mutual (over 99%). A1 makes up about 80% of all A-type blood, with A2 making upwards almost all of the rest.[37] These 2 subgroups are not ever interchangeable as far as transfusion is concerned, as some A2 individuals produce antibodies against the A1 antigen. Complications can sometimes ascend in rare cases when typing the blood.[37]

With the evolution of Dna sequencing, it has been possible to place a much larger number of alleles at the ABO locus, each of which can be categorized equally A, B, or O in terms of the reaction to transfusion, but which can be distinguished past variations in the Deoxyribonucleic acid sequence. In that location are 6 common alleles in white individuals of the ABO gene that produce one's blood type:[38] [39]

A B O
A101 (A1)
A201 (A2) 		B101 (B1) O01 (O1)
O02 (O1v)
O03 (O2)

The same report also identified xviii rare alleles, which mostly have a weaker glycosylation activity. People with weak alleles of A tin can sometimes express anti-A antibodies, though these are usually not clinically significant as they practise not stably interact with the antigen at trunk temperature.[40]

Cis AB is another rare variant, in which A and B genes are transmitted together from a single parent.[ citation needed ]

Distribution and evolutionary history [edit]

The distribution of the blood groups A, B, O and AB varies across the world co-ordinate to the population. There are also variations in blood type distribution within man subpopulations.[ citation needed ]

In the United kingdom, 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 Celts, Norsemen, Danes, Anglo-Saxons, and Normans who contributed the morphemes to the placenames and the genes to the population. The native Celts tended to have more type O blood, while the other populations tended to have more blazon A.[41]

The ii mutual O alleles, O01 and O02, share their starting time 261 nucleotides with the group A allele A01.[42] However, different the group A allele, a guanosine base is after deleted. A premature stop codon results from this frame-shift mutation. This variant is constitute worldwide, and probable predates human being migration from Africa. The O01 allele is considered to predate the O02 allele.[ citation needed ]

Some evolutionary biologists theorize that there are four chief lineages of the ABO cistron and that mutations creating type O take occurred at least three times in humans.[43] 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 outcome of balancing selection.[43] Both theories contradict the previously held theory that type O blood evolved first.[ citation needed ]

Origin theories [edit]

It is possible that food and environmental antigens (bacterial, viral, or plant antigens) have epitopes similar plenty to A and B glycoprotein antigens. The antibodies created confronting these environmental antigens in the showtime years of life can cross-react with ABO-incompatible red blood cells that information technology comes in contact with during claret transfusion later in life. Anti-A antibodies are hypothesized to originate from allowed response towards influenza virus, whose epitopes are like enough to the α-D-N-galactosamine on the A glycoprotein to be able to elicit a cross-reaction. Anti-B antibodies are hypothesized to originate from antibodies produced against Gram-negative leaner, such as Eastward. coli, cross-reacting with the α-D-galactose on the B glycoprotein.[44]

Nonetheless, it is more probable that the strength driving evolution of allele variety is simply negative frequency-dependent selection; cells with rare variants of membrane antigens are more easily distinguished past the immune system from pathogens carrying antigens from other hosts. Thus, individuals possessing rare types are better equipped to detect pathogens. The high within-population diversity observed in homo populations would, then, exist a consequence of natural selection on individuals.[45]

Clinical relevance [edit]

The carbohydrate molecules on the surfaces of red blood cells have roles in cell membrane integrity, cell adhesion, membrane transportation of molecules, and acting equally receptors for extracellular ligands, and enzymes. ABO antigens are establish having similar roles on epithelial cells likewise as scarlet claret cells.[46] [47]

Bleeding and thrombosis (von Willebrand factor) [edit]

The ABO antigen is also expressed on the von Willebrand cistron (vWF) glycoprotein,[48] which participates in hemostasis (command of bleeding). In fact, having type O claret predisposes to bleeding,[49] as xxx% of the full genetic variation observed in plasma vWF is explained by the event of the ABO blood group,[fifty] and individuals with grouping O blood normally have significantly lower plasma levels of vWF (and Cistron VIII) than do non-O individuals.[51] [52] In addition, vWF is degraded more rapidly due to the higher prevalence of blood group O with the Cys1584 variant of vWF (an amino acrid polymorphism in VWF):[53] the gene for ADAMTS13 (vWF-cleaving protease) maps to human being chromosome 9 band q34.2, the same locus equally ABO blood blazon. Higher levels of vWF are more common amongst people who have had ischemic stroke (from claret clotting) for the starting time time.[54] The results of this study found that the occurrence was not affected by ADAMTS13 polymorphism, and the only pregnant genetic factor was the person's blood group.[ citation needed ]

ABO hemolytic affliction of the newborn [edit]

ABO claret group incompatibilities between the mother and child does not ordinarily cause hemolytic affliction of the newborn (HDN) considering antibodies to the ABO claret 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 infant tin potentially develop ABO hemolytic disease of the newborn.[ citation needed ]

Clinical applications [edit]

In human cells, the ABO alleles and their encoded glycosyltransferases have been described in several oncologic atmospheric condition.[55] Using anti-GTA/GTB monoclonal antibodies, it was demonstrated that a loss of these enzymes was correlated to cancerous float and oral epithelia.[56] [57] Furthermore, the expression of ABO blood grouping antigens in normal homo tissues is dependent the blazon of differentiation of the epithelium. In most human carcinomas, including oral carcinoma, a significant effect as part of the underlying machinery is decreased expression of the A and B antigens.[58] Several studies have observed that a relative down-regulation of GTA and GTB occurs in oral carcinomas in association with tumor development.[58] [59] More than recently, a genome wide association study (GWAS) has identified variants in the ABO locus associated with susceptibility to pancreatic cancer.[60] In improver, another large GWAS report has associated ABO-histo blood groups also as FUT2 secretor condition with the presence in the abdominal microbiome of specific bacterial species. In this case the clan was with Bacteroides and Faecalibacterium spp. Bacteroides of the same OTU (operational taxonomic unit) have been shown to be associated with inflammatory bowel disease,[61] [62] thus the written report suggests an important role for the ABO histo-blood group antigens as candidates for direct modulation of the human microbiome in wellness and disease.[63]

Clinical marker [edit]

A multi-locus genetic adventure score study based on a combination of 27 loci, including the ABO gene, identified individuals at increased adventure for both incident and recurrent coronary artery disease events, equally well as an enhanced clinical benefit from statin therapy. The study was based on a customs cohort report (the Malmo Diet and Cancer study) and iv boosted randomized controlled trials of primary prevention cohorts (JUPITER and ASCOT) and secondary prevention cohorts (Care and Evidence IT-TIMI 22).[64]

Amending of ABO antigens for transfusion [edit]

In April 2007, an international team of researchers appear in the journal Nature Biotechnology an inexpensive and efficient way to convert types A, B, and AB blood into type O.[65] This is washed by using glycosidase enzymes from specific bacteria to strip the claret group antigens from red blood cells. The removal of A and B antigens even so does not address the problem of the Rh blood group antigen on the blood cells of Rh positive individuals, and so blood from Rh negative donors must be used. The sort of claret is named "enzyme converted to O" (ECO) claret. Patient trials will be conducted earlier the method can exist relied on in live situations. One such Phase 2 trial was done on B-to-O blood in 2002.[66]

Some other approach to the blood antigen problem is the industry of artificial claret, which could act equally a substitute in emergencies.[67]

Pseudoscience [edit]

During the 1930s, connecting blood groups to personality types became popular in Japan and other areas of the world.[68] Studies of this association accept yet to ostend its being definitively.[69]

Other pop but unsupported ideas include the use of a claret type nutrition, claims that group A causes astringent hangovers, group O is associated with perfect teeth, and those with claret group A2 take the highest IQs. Scientific evidence in support of these concepts is limited at all-time.[70]

Meet also [edit]

  • Secretor status – secretion of ABO antigens in body fluids

References [edit]

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Further reading [edit]

  • Dean Fifty (2005). "Chapter 5: The ABO claret group". Blood Groups and Red Prison cell Antigens . Retrieved 24 March 2007.
  • Farr A (1 April 1979). "Blood group serology--the outset iv decades (1900–1939)". Med Hist. 23 (2): 215–26. doi:10.1017/s0025727300051383. PMC1082436. PMID 381816.

External links [edit]

  • ABO at BGMUT Blood Grouping Antigen Gene Mutation Database at NCBI, NIH
  • Encyclopædia Britannica, ABO claret group system
  • National Blood Transfusion Service
  • Molecular Genetic Basis of ABO

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Source: https://en.wikipedia.org/wiki/ABO_blood_group_system

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