ABO Blood Group System

For example, the ABO blood group system has three alleles that bear upon the expression of antigens on the surface of red blood cells: alleles A, B, and O. Both alleles A and B are expressed in individuals with the AB claret blazon.


Brenner’s Encyclopedia of Genetics (2nd Edition)

ABO Claret Grouping System

, in

Encyclopedia of Immunology (2d Edition), 1998

ABO antibodies

The clinical importance of the
ABO blood group system
derives from the universality of its antibodies and their

in vivo
say-so. The ‘naturally occurring’ antibodies of the majority of group A or B individuals are mainly IgM and produced in response to environmental ABO antigens, e.g. from microbes in the gut and respiratory tract. Such IgM antibodies, although displaying optimal activity in the cold, are reactive at 37°C and tin actuate the complement cascade up to the C9 phase, leading to the immediate intravascular lysis of transfused incompatible reddish cells
in vivo. In the Uk, roughly 1 in every iii randomly selected, ungrouped blood donations would exist incompatible with a given recipient; such incompatible transfusions can pb to renal failure, disseminated intravascular coagulation and even death. The majority of the signs and symptoms of severe ABO hemolytic transfusion reactions tin can be attributed to the generation of C3a and C5a fragments as a result of complement fixation, with the consequent release of vasoactive amines from mast cells and of cytokines such as interleukin-1 (IL-one), IL-6, IL-8 and tumor necrosis cistron α (TNFα) from mononuclear cells.

Virtually, if non all, group O adults, and a small proportion of group A and B subjects, have naturally occurring, unremarkably weak, IgG in addition to stronger IgM ABO antibodies. The IgG component can cross the placenta and bind to fetal red cells; however, lysis of fetal red cells is by and large minimal and hemolytic affliction of the newborn (HDN) caused past ABO antibodies is usually mild or inapparent in Western Europe and Due north America. The occurrence of HDN due to ABO antibodies cannot be predicted, just information technology only affects the offspring of group O mothers. The lack of severity of about cases of ABO HDN is thought to be due to: 1) IgG ABO antibodies being predominantly IgG2, which is incapable of initiating complement-mediated hemolysis or devastation of antibody-coated ruby-red cells by the mononuclear phagocytic system (many sera have IgG1 ABO antibodies as well every bit an IgG2 component; a few sera have trace amounts of IgG3 and IgG4 antibodies); two) substantial amounts of maternal IgG ABO antibodies binding to ABO sites on tissues other than red cells in the fetus; 3) soluble ABH antigens in plasma and trunk fluids of the fetus which neutralize IgG anti-A and anti-B and inhibit their binding; 4) the ABO epitopes of fetal red cells existence nowadays on unbranched oligosaccharides, which are thought to be unable to back up the divalent IgG bounden needed for complement activation past IgG1 or IgG3 antibodies; 5) fetal complement levels existence too depression to support efficient lysis of string (or even adult) target red cells. All the same, in some parts of the world, ABO HDN is often more than severe and this is attributed to environmental factors such every bit the stimulation of ABO antibodies past microbes and parasites.

Some individuals possess plasma IgA ABO antibodies irrespective of immunization; ABO antibodies of colostrum are often wholly IgA, although sometimes IgM antibodies can also be institute.

String blood commonly does not contain ABO antibodies although maternally derived IgG anti-A or -B can sometimes be detected. Newborn infants do not produce ABO antibodies until the 3rd-6th month of historic period (median titer = 4), reaching a maximal titer (approx. = 128) between the ages of 5 and 10 years. Anti-A seems to attain higher titers more rapidly than anti-B. Adult titers of anti-A range from 32 to 2048 (median = 256) and anti-B from 8 to 512 (median = 64). The vast bulk of healthy adults have readily detected ABO antibodies. Weakening of ABO antibodies tin can occur naturally in individuals aged over 50; a third of patients over 65 have ABO antibiotic titers of iv or less. Occasional subjects may lack the appropriate ABO agglutinins, especially if hypogammaglobulinemic, or if their plasma IgM levels are low. Antibodies can be lost by exhaustive plasma substitution (used therapeutically in ABO incompatible bone marrow and organ transplantation) or by immunosuppression caused by therapy or by disease. IgM anti-A or -B are completely absent in individuals with the very rare Wiskott-Aldrich syndrome.

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ABO Claret Group System

Marion E.
PhD, FIBMS, DSc (Hon.)
, …
Martin L.
, in

The Claret Group Antigen FactsBook (3rd Edition), 2012

Molecular basis associated with A antigen

Come across
ABO Blood Grouping System
folio for genetic basis of A subgroups.

Event of enzymes and chemicals on A antigen on intact RBCs
Ficin/Papain Resistant (markedly enhanced)
Trypsin Resistant (markedly enhanced)
α-Chymotrypsin Resistant (markedly enhanced)
DTT 200
Acid Resistant

In vitro

characteristics of alloanti-A
Immunoglobulin class IgM; IgG
Optimal technique RT or below; IAT for IgG component^
Neutralization Saliva from A secretors
Complement binding Yes; some hemolytic
May be particularly relevant when testing or titrating the sera of platelet donors, pregnant women, and patients waiting for or having undergone ABO-incompatible organ transplantation or following ABO-not-identical stem cell transplantation complicated by pure red jail cell aplasia due to anti-A.
Clinical significance of alloanti-A
Transfusion reaction None to severe; immediate/delayed; intravascular/extravascular
HDFN No to moderate (rarely severe)

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Perinatal Alloantibody Disorders – Neonatal Alloimmune Thrombocytopenia/Hemolytic Disease of the Fetus and Newborn

, in

Reference Module in Biomedical Sciences, 2014

Other Antigens as Causes of HDFN

ABO Incompatibility

ABO blood group system
is unique in that it is amid the merely human antigen organisation in which antibodies to nonnative antigens develop naturally; prior exposure to foreign erythrocytes (sensitization) is not required. Therefore, ABO incompatibility tin can affect a first incompatible pregnancy. Information technology is estimated that ABO incompatibility affects equally many as xv–twenty% of pregnancies, merely less than 1% of all pregnancies are complicated past ABO-induced HDFN. HDFN due to ABO incompatibility is by and large substantially less astringent than Rh illness, and is not typically associated with fetal hydrops (only isolated cases ever reported) or fetal demise. Affected infants are typically non anemic or have very mild anemia, and have varying degrees of hyperbilirubinemia that can present <24 h of life and may require phototherapy. Serious complications such every bit kernicterus are quite rare. Neonatal IVIG has been shown to reduce the degree of jaundice, which may be clinically significant despite typically not causing a big numerical difference.

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Immunology Guidebook, 2004

ABO claret grouping arrangement

ABO blood group system
is the first described of the human blood groups based upon carbohydrate alloantigens nowadays on red jail cell membranes. Anti-A or anti-B isoagglutinins (alloantibodies) are present only in the claret sera of individuals not possessing that specificity. This serves as the basis for grouping humans into phenotypes designated A, B, AB, and O. Blood group methodology to determine the ABO blood blazon makes use of the agglutination reaction.

Tabular array 15.2

shows ABO blood group antigens, antibodies, and the front end and back typing.

Table 15.ii.
ABO blood group antigens, antibodies and grouping past front and back typing

Front typing Back typing
Reaction of cells tested with Reaction of serum tested against
Blood type Erythrocyte surface antigen Antibody in serum Anti-A Anti-B A cells B cells O cells
A A antigen Anti-B + +
B B antigen Anti-A + +
AB A, B antigens No antibody + +
O H antigen Both anti-A and anti-B + +

The ABO system remains the most important in the transfusion of blood and is also disquisitional in organ transplantation.

Table 15.3

gives the suggested ABO grouping selection order for transfusion of erythrocytes and plasma. Epitopes of the ABO system are found on oligosaccharide final sugars. The genes designated equally
A/B, Se, H, and
govern the formation of these epitopes and of the Lewis (Le) antigens. The ii precursor substances type I and type II differ merely in that the last galactose is joined to the penultimate N-acetylglucosamine in the b ane–three linkage in blazon I chains, but in the b 1–4 linkage in type II chains.

Tabular array 15.three.
Suggested ABO group choice gild for transfusion of erythrocytes and plasma

Component ABO group
1st choice 2nd option 3rd option 4th choice
Recipient ABO grouping RBC Plasma RBC Plasma RBC Plasma RBC Plasma
AB AB AB A (A) B (B) O (O)
A A A O AB (B) (O)
B B B O AB (A) (O)

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Coevolution of Humans and Pathogens

, in

Nuts in Human Evolution, 2015

ABO Blood Groups and Infectious Diseases

ABO blood grouping system
was the first biochemical genetic polymorphism detected in humans. Frequencies of the alleles in this genetic system vary markedly beyond space, and evolutionary explanations have been proposed to explain this variation since the system’s discovery past Karl Landsteiner in the early on 1900s. The ABO system was offset recognized as a consequence of studies to determine why blood transfusions were sometimes successful and at other times unsuccessful.

Landsteiner (1900)
showed that human blood could be classified into unlike types on the footing of whether the mixing of two samples of blood led to clumping (agglutination). This agglutination occurred when donors and recipients had certain types of unmatched blood, and resulted from an antigen–antibody response that occurred when the recipient produced antibodies to fight off the foreign antigens nowadays on a donor’s blood cells. Recognition of the ABO claret types, and subsequent efforts to match them when giving transfusions, greatly improved the success rates of the procedures.

The molecular ground of the ABO claret system was start proposed past
Yamamoto et al. (1990). The ABO gene codes for a glycosyltransferase (an enzyme) that facilitates the addition of a saccharide to the end of a forerunner antigen, the H antigen, on the surface of red claret cells. The system consists of 3 alleles, A, B, and O. Presence of the A allele causes the glycosyltransferase to attach the sugar
Due north-acetyl
d-galactosamine to the H antigen, converting it to the A antigen; the B allele’due south presence causes the glycosyltransferase to attach a different saccharide,
d-galactose, converting it to the B antigen. The O allele causes the glycosyltransferase gene to become inactivated; thus, individuals who possess only O alleles (i.e., have blood type O) practice non alter the H antigen and and so have neither A nor B antigens on the surface of their red claret cells (Anstee, 2010; Yamamoto et al., 1990). The A, B, and H antigens are not limited to just ruby blood cells, only are found in a diverseness of other cells in the body (Anstee, 2010).

As a result of the medical importance of the ABO blood grouping system, abundant data are available on the worldwide frequencies of the A, B, and O alleles. At the worldwide level, the O allele is about mutual and occurs about 63% of the time, the A allele occurs 21% of the time, and the B allele occurs near xvi% of the time. Yet, in that location is extensive geographic variation. For example, the B allele is virtually mutual amid individuals of Asian ancestry, but information technology is nearly absent-minded among pure-blooded indigenous N and South Americans, fifty-fifty though many other genetic traits signal that these populations originated in Asia (Brues, 1977; Cavalli-Sforza et al., 1994).

The loftier degree of genetic variability in the ABO system in all human populations outside of the New Earth is as well high to be explained by recurrent mutation (see Futuyma in this volume). Thus, hypotheses nearly the roles of other evolutionary forces take been repeatedly proposed. For example, the ubiquitous presence of the O allele in most pure-blooded ethnic Northward and South Americans is often suggested to be a consequence of founder event and subsequent genetic
drift occurring in the undoubtedly small groups that migrated into the New World from Asia. It is important to annotation, however, that the evidence for multiple migrations from Asia to the New World reduces the gamble that founder effect and genetic migrate alone are responsible, since these processes would be just as likely to result in high frequencies of either the A or the B allele in different groups.
Matson and Schrader (1933)
observed that Blackfeet and Blood Indians in northwestern North America have a much higher frequency of the A allele than do other Amerindian groups, maybe because genetic drift in these groups resulted in an increase of the A allele relative to the O allele rather than extinction of the A and B alleles (Szathmary and Auger, 1983).

Natural option has also often been proposed as an explanation for the distribution of ABO claret groups. Often the option arguments have posited that interactions of human being groups with infectious diseases may exist responsible for the observed variation, although noninfectious diseases are too commonly implicated (Table 2).

Table 2.
Known and Proposed Associations betwixt ABO Blood Type and Human Disease

Disease/Pathogen Implicated Selected References
I. Associations with Infectious Diseases
Helicobactor pylori, peptic ulcer Alkout et al. (2000)
Edgren et al. (2010)
Malaria Cserti and Dzik (2007)
Zerihun et al. (2011)
Cholera Glass et al. (1985)
Harris et al. (2005)
E. coli Blackwell et al. (2002)
Hutson et al. (2002)
Tan and Jiang (2005, 2010)
Pettenkofer et al. (1962)
Chakravartti et al. (1966)
Vogel et al. (1960)
Pettenkofer et al. (1962)
II. Associations with Other Diseases
Arterial and venous thromboembolism Anstee (2010)
Salivary and gastric cancer Aird et al. (1953)
Edgren et al. (2010)
Exocrine pancreatic cancer
Iodice et al. (2010)
Wang et al. (2012)
Resistance to norovirus infection depends on man histo-blood group antigens, which are related to secretor and Lewis alleles in improver to ABO alleles.
The associations of smallpox and plague with ABO blood groups are among the first proposed relationships between claret groups and affliction, but the thought is now controversial (Anstee, 2010).

Wang et al. (2012)
suggested that interactions between hepatitis B virus and ABO blood type may play a role in the development of pancreatic cancer.

Many of the arguments related to infectious diseases swivel on the recognition that some kinds of infectious pathogens possess antigens on the surface of their cells that are similar in structure to the A or B antigens on homo red claret cells. Persons possessing the A and/or B antigens on their red blood cells do not mount antibody responses against those cells (which otherwise would destroy their own blood) so the argument is that they likewise cannot recognize pathogens that incorporate similar antigens. For example, the smallpox virus possesses an antigen like to the A antigen on cerise claret cells. Thus, the immune organisation of individuals who have A or AB blood type may not be able to recognize the smallpox virus likewise equally individuals who have B or O blood type, and may accept been selected confronting during smallpox epidemics. Although this is an attractive hypothesis, it remains controversial, largely because results of studies looking at whether there was an observed relationship in the postulated management have been mixed (Mielke et al., 2011). A similar statement related to the carmine blood cell H antigen described above was proposed to explain a relatively low frequency of the O allele in parts of Europe and Asia, and additional relationships between infectious diseases and the frequency of the ABO alleles in different locations take been proposed (Mielke et al., 2011). The observed relationships between malaria, cholera,
Helicobactor pylori, and norovirus mentioned in
Table 2
do seem to exist solid, but in full general the associations have not been adequate to fully assess whether infectious diseases have played of import roles in generating the observed distributions of the ABO alleles.

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The RBC as a Target of Damage

, in

Pathobiology of Human Disease, 2014

Non-ABO incompatibility

In addition to the
ABO blood group organisation, the RBC membrane possesses hundreds of non-ABO antigens which serve numerous functional purposes. Over the by 70–eighty years, a subset of these non-ABO antigens accept been well characterized because of their clinical significance in the setting of transfusion medicine. Antigens within blood grouping systems such equally Rh, Kell, Kidd, Duffy, and MNSs all represent potential immunologic targets for alloantibody development (

Table 3
). Inside given blood group systems, well-nigh clinically pregnant non-ABO antigens differ by only a single amino acid (e.thousand., Jka
vs. Jkb
in the Kidd blood grouping system), yet this small structural difference is substantial enough to allow an private lacking one particular antigen to form an alloantibody against it with a transfusion exposure.

Table three.
Immunologic and transfusion characteristics of clinically significant not-ABO blood group antigens and alloantibodies

Blood group system Antigens Alloantibody frequency Associated with DHTRs?


Associated with HDFN?
Rh D Very common Yep (rare) Yeah
E Very common Yep Yes
C Very common Yes Yes
c Common Yep Yes
Kell K Very mutual Yep Yep
Kidd Jka Common Yep Yep
Jkb Mutual Aye Yes (rare)
Duffy Fya Common Yeah Yes
Fyb Rare Yes Yes (rare)
MNSs M Common Yes No
North Rare Yes (rare) No
Southward Common Yeah Yes (rare)
s Common Yes Yes (rare)
Lewis Lea Common Yes (rare) No
Leb Common Yes (rare) No
P P1 Rare Aye (rare) No
Delayed hemolytic transfusion reaction.

Different the ABO arrangement where alloantibodies are ‘naturally occurring,’ virtually all non-ABO antigens require exposure to a foreign antigen through transfusion or pregnancy earlier alloimmunization is observable. Moreover, the immunogenicity of not-ABO antigens is highly variable, with some antigens (e.chiliad., D and K) requiring only a single exposure before an antibody is developed, while for others (e.chiliad., Fyb), repeated exposures may never lead to development of an alloantibody. Contempo human studies have suggested that claret group antigen immunogenicity may be tied in part to an individuals’ grade II HLA expression. Even so, antigens such equally RhD are not homo leukocyte antigen (HLA) restricted, potentially due to its large size. Much work remains to be completed to determine what factors contribute to a particular antigen’s immunogenicity in a item transfusion recipient. Further details on brute model work done to improve enhance our agreement of the factors contributing to non-ABO claret group antigen alloimmunization are discussed later on in this commodity.

Given the variable immunogenicity of not-ABO antigens, and the possibility that only a subset of transfusion recipients may be capable of responding to a given antigen, non-ABO antibodies are somewhat uncommon overall in the general patient population. Large-scale studies have shown that about ii–3% of all patients undergoing IAT for transfusion possess these antibodies. When non-ABO antibodies are documented, they are typically of IgG class and infrequently set up complement. Therefore, if a patient with an underlying non-ABO alloantibody is inadvertently transfused with an incompatible RBC unit, the resulting hemolysis is most often extravascular with symptoms consisting of mild anemia, fever, and jaundice. Such extravascular reactions are associated with DATs showing agglutination with AHG and, much less oftentimes, anti-C3. As with the ABO system, appropriate safety and quality systems can help claret banks and transfusion services to place near patients with not-ABO antibodies and provide them with compatible, antigen-negative RBC units.

Information technology is of import to note that a unique holding of non-ABO antibodies, termed ‘evanescence,’ tin complicate testing regimens for some alloimmunized patients and raise their risks for suffering an adverse transfusion event. With evanescence, the titer of such antibodies decreases below the level of detection with a risk that incompatible RBC units may be inadvertently transfused. Upon reexposure to RBC units containing the cognate antigen against which an individual was previously alloimmunized, patients will often undergo an immunologic anamnestic retention response days to weeks later. As their IgG-class non-ABO antibodies increment in titer following this secondary exposure, these patients experience a miracle known as a delayed extravascular hemolytic reaction (and then named because the signs and symptoms of hemolysis occurs substantially later the transfusion exposure, as opposed to the acute reactions seen in ABO-incompatible transfusions). Delayed reactions present similar to other extravascular forms of hemolysis, and are typically associated with mild anemia, fever, and jaundice. Since such reactions are due to an inability to detect non-ABO blood group alloantibodies at the time of pretransfusion testing, their prevention revolves effectually increased portability of wellness information. Several studies have shown that the use of local or regional non-ABO blood grouping antibiotic databases can help disseminate claret group antibody history and allow for the provision of uniform units to patients who are no longer demonstrating their blood grouping alloantibodies.

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https://world wide web.sciencedirect.com/science/article/pii/B9780123864567062031

Homo Genome Diversity and its Value

, in

International Encyclopedia of the Social & Behavioral Sciences, 2001



The era of modern genetics began with the rediscovery of Mendel’s laws in 1900. All the same, long before this rediscovery, Charles Darwin (1859) recognized that variation in characteristics among individuals provided the footing of origin of species. Evolutionary biologists and population geneticists accept long been interested in studying such variations, especially those that have genetic bases, and their origins and maintenance. Genomic diversity of a population is the raw material for its evolution by natural choice. Genomic variety of a population can exist measured in several ways. The most unremarkably used measure out is the probability that 2 genes at whatever particular position of the chromosomes chosen randomly from the population are dissimilar. Of course, it is not practically possible to choose genes, since at any position of the chromosomes, ii genes remain in combination in an individual. The above probability is equivalent to the probability that if an individual is drawn at random, this individual volition possess a combination of two different genes at the chromosomal location nether consideration. The different gene variants at any chromosomal location (locus) are called alleles. The combination of two alleles at a locus in an individual is chosen the genotype of the individual. When the genotype comprises the aforementioned ii identical alleles, information technology is said to exist homozygous; otherwise, heterozygous. The higher this probability, the greater is the genomic diversity. When all individuals of a population accept identical genes, this probability attains the value of zero indicating that there is no genomic multifariousness in the population at that locus.


The Beginning of Human Genome Diverseness Studies

The fact that individuals can differ in inherited traits was offset conspicuously established with the identification of the
ABO blood grouping system
by Landsteiner in 1900. Soon afterwards Earth War I, the Hirschfelds (

1919) start discovered that human populations differ in frequencies of ABO claret group types. This finding marked the beginning of human being genome diversity studies. Subsequently, the development of biochemical- and molecular-genetic techniques accept provided greater understanding and more refined estimates of human genome variety.


The Importance of Genetic Variety

It is crucial for any population to be genetically diverse. Humans, like many other species, are susceptible to various infections, many life-threatening. At that place is an increasing realization from contempo research that genetic factors are involved in conferring susceptibility/resistance to most such infections. If all individuals in a population were to be genetically the same, then in the outcome of an outbreak of a new infection, information technology is possible for the entire population to be easily wiped out by the infectious agent if no private carries genes conferring resistance to this amanuensis.

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Autosomal Inheritance

, in

Brenner’south Encyclopedia of Genetics (Second Edition), 2013

Autosomal Codominant Inheritance

Autosomal codominant inheritance refers to two alleles of an autosomal gene where each allele contributes to the phenotype. For instance, the
ABO blood group organization
has three alleles that affect the expression of antigens on the surface of red blood cells: alleles A, B, and O. Both alleles A and B are expressed in individuals with the AB blood type. A and B alleles are considered codominant with respect to each other. Blood group O is recessive to A and B because individuals with AA or AO alleles have an A phenotype and individuals with BB or BO alleles accept a B phenotype.

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https://www.sciencedirect.com/scientific discipline/article/pii/B9780123749840001212


, in

Encyclopedia of Genetics, 2001

Blood Groups Polymorphism

Ane of the most commonly known genetic polymorphisms is that of the scarlet blood prison cell antigens in humans. We all know near the
ABO blood group system
which has iii alleles and gives rise to vi genotypes but only iv phenotypes (the four claret groups): A, B, AB, and O. The A and B blood group individuals can be either homozygous or heterozygous. Blood groups are defined on the basis of chemic cues on the surface of the claret cells (antigens) which are involved in prison cell recognition. Only certain combinations of blood transfusions are possible. More than xx blood group genes are known but only a few of these are highly polymorphic (e.g., MNS, Rh

, Kidd, Duffy, and Lutheran). One of the most circuitous and polymorphic factor systems in humans is the ‘major histocompatibility circuitous’ (MHC), the HLA system, on chromosome half dozen, where scores of genes are involved. These genes are and then highly polymorphic that no two individuals (except identical twins) are alike in their HLA genotypes. Some of the blood group genes (such as rhesus, Lutheran, and Kell) show allele frequency variation between human being populations and are of anthropological interest in human studies.

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Genes in Families

, in

Emery and Rimoin’s Principles and Exercise of Medical Genetics and Genomics (Seventh Edition), 2019



If the phenotype of AB displays the phenotypic features of both the homozygotic states, then alleles A and B are said to be codominant. The human
ABO blood group organisation
exhibits codominance. The system consists of 3 alleles A, B, and O. Both A and B are dominant in relation to O, and therefore blood group A can accept the genotype AA or AO. Claret group B can have the genotype BB or BO. However, neither A nor B shows dominance over the other, and therefore individuals with the genotype AB have the phenotypic characteristics of both blood group A and blood grouping B.

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