Biochemical basis and genetics
The antigen profile of the major AB0 blood group system is determined by three codominant alleles: H, A and B.
The basic building block for all antigens of this group is H substance—a universal precursor molecule. What it turns into depends on the activity of specific genes:
- Gene H stops further chemical transformation. The precursor molecule remains unchanged.
- Genes A and B trigger the synthesis of specific enzymes (glycosyltransferases). These enzymes modify the H molecule by attaching new carbohydrate residues to it, creating unique antigenic epitopes.
Biochemical differences between antigens:
- Antigen A is the result of adding a D-N-acetylgalactosamine residue to H substance.
- Antigen B is the result of adding a D-galactose residue to H substance.
Phenotypes and nomenclature
In medicine, blood groups are conventionally designated by a combination of a Roman numeral and a phenotypic letter code. The formation of a specific group directly depends on the expression of carbohydrate antigens on erythrocytes:
- Group I(0): only H substance is present on the cells. Specific antigens A and B are completely absent.
- Group II(A): erythrocytes carry antigen A. If the patient has the A/h genotype, antigen A is expressed together with H substance.
- Group III(B): erythrocytes carry antigen B. With the B/h genotype, it is also detected in combination with H substance.
- Group IV(AB): heterozygote phenotype (A/B) in which both antigens—A and B—are simultaneously expressed on the membrane.
Natural antibodies and compatibility
A fundamental feature of the AB0 system that plays a critical role in blood transfusions is the presence of natural antibodies in the serum. The body always produces antibodies against those erythrocyte antigens that are absent from its own cells. These are precisely what cause incompatibility and the destruction of donor erythrocytes in transfusion errors.
Summary of phenotypes and antibodies:
| Group | Genotype | Antigen on erythrocytes | Antibodies in serum |
|---|---|---|---|
| 0(I) | h/h | H | Anti-A (α), anti-B (β) |
| A(II) | A/A, A/h | A | Anti-B (β) |
| B(III) | B/B, B/h | B | Anti-A (α) |
| AB(IV) | A/B | A, B | Absent |
Briefly: answers to topical questions
What rare variants and the Bombay phenotype exist in the AB0 system?
The Bombay phenotype is an example of epistatic interaction of non-allelic genes, in which blood group I (0) is always formed.
- H gene (H) is the dominant allele responsible for the synthesis of the precursor molecule for antigens A and B.
- h gene (h) is a recessive allele that does not provide synthesis of the precursor.
In recessive homozygotes for the h gene (hh genotype), antigens A and B are not formed on erythrocytes. This occurs even if alleles encoding enzymes to create antigens A or B are present in the genotype.
What other major erythrocyte alloantigen systems, besides AB0, are considered in clinical practice?
Besides the AB0 system, other blood group systems exist, including the Rhesus system, Kell, Duffy, MNS, P, Lutheran (Lu), and Diego. In maternal-fetal incompatibility, the Rhesus factor can be the underlying cause; Kell and Duffy systems are rarely involved. The AB0, Rh, MN, Duffy, and Diego systems are also used in phylogenetic studies.
To memorize the biochemistry: Antigen A — Acetylgalactosamine (both start with A). Antigen B — Galactose.
Class and exam questions
Which molecule serves as the common basis for all AB0 system antigens?
The common precursor molecule is H substance. In the presence of genes A or B, additional sugars attach to it.
Which enzymes are responsible for the formation of antigens A and B?
Glycosyltransferases are responsible for this process. They catalyze the reaction of attaching specific carbohydrate residues to the precursor molecule.
Why is it impossible to transfuse blood group A(II) to a recipient with group 0(I)?
The blood serum of an individual with group 0(I) contains natural anti-A (α) antibodies. Upon contact with group A donor erythrocytes, they will cause an immune conflict.
What else to study on this topic
- Mechanism of lectin binding to erythrocyte polysaccharides
- Detailed biochemical pathway of H substance synthesis
- Clinical consequences of transfusion incompatibility
- Other erythrocyte alloantigen systems (besides AB0)
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