General characteristics and antigen localization
The antigenic properties of blood cells depend on specific chemical structures on their surface. These structures are based on oligosaccharides that are part of the glycoprotein complexes of the outer cell membrane.
In immunohematology, several systems classify blood according to these characteristics, but two are considered fundamental:
- AB0 system — is of critical importance in blood transfusion and the development of immune conflicts.
- Rhesus system — divides all people into two categories: Rhesus-positive and Rhesus-negative.
It is important to note that blood group antigens are not exclusive to erythrocytes. They are also expressed on the membranes of platelets, cells of various body tissues, and are even secreted in bodily fluids such as saliva, breast milk, and seminal fluid.
Characteristics of AB0 blood groups
The AB0 system is based on the presence of two types of protein structures: antigens (agglutinogens) located on the erythrocyte membrane, and antibodies (agglutinins) circulating in the blood plasma. Depending on their combination, four main groups are distinguished:
- Group I (0)
Only the baseline 0 antigen is present on the erythrocyte surface. The blood plasma contains two types of antibodies simultaneously: anti-A and anti-B. This is the most common group, occurring in approximately 40% of people.
- Group II (A)
Erythrocytes carry the baseline 0 antigen and antigen A. Only anti-B antibodies are produced in the plasma. This phenotype is the most frequent, covering about 43% of the population.
- Group III (B)
Antigens 0 and B are located on the membrane of red blood cells. The plasma contains anti-A antibodies. This group is less common—about 12% of people are carriers.
- Group IV (AB)
Blood cells are equipped with a full set of antigens: 0, A, and B. At the same time, group antibodies are completely absent in the plasma. This is the rarest group, characteristic of only 5% of the population.
Mechanisms of group incompatibility
Group incompatibility is the basis of severe complications during blood transfusion. The essence of the pathological reaction is agglutination—the clumping of erythrocytes into conglomerates, which is inevitably followed by their destruction (hemolysis).
This process is triggered when corresponding antigens and antibodies meet in the bloodstream (for example, antigen A encounters anti-A). In clinical practice, two vectors of immune attack are distinguished:
- Recipient attack: the patient's own antibodies destroy donor erythrocytes. This is the most common and dangerous mechanism of incompatibility.
- Donor attack: antibodies contained in the transfused donor plasma attack the patient's erythrocytes (occurring predominantly during whole blood transfusion).
A clear example of incompatibility is the mixing of blood of groups II (A) and III (B). In this case, a massive cross-reaction is triggered: the recipient's anti-B antibodies bind to the donor's B-erythrocytes, and the donor's anti-A antibodies attack the recipient's A-erythrocytes.
Principles of blood transfusion
During small-volume blood transfusions, the dilution rule applies: when donor antibodies (agglutinins) enter the recipient's bloodstream, they are repeatedly diluted by the recipient's plasma, causing their concentration to drop below a critical level so that they cannot damage the patient's cells.
Based on this, the main rule of safe transfusion is to prevent the interaction of recipient antibodies with the introduced donor erythrocytes.
Basic compatibility rules for small volumes:
- Bearers of Group I (0) are considered universal donors, as their erythrocytes lack antigens A and B, meaning they can be transfused to people with any blood group.
- People with Group IV (AB) are universal recipients, since their plasma lacks antibodies capable of attacking foreign erythrocytes.
- Blood of groups II (A) and III (B) is permitted for transfusion to patients with the exact same blood group, or to recipients with group IV (AB).
Briefly: answers to topical questions
What other erythrocyte antigen systems exist besides AB0 and the Rhesus factor?
In addition to the AB0 and Rhesus systems, more than 200 different antigens are present on erythrocyte membranes. Sources additionally mention other systems/antigens and rare (minor) factors:
- Kell: K, k, Kpa, Kpb.
- Duffy: Fya, Fyb.
- Lewis.
- MNS.
- Jka, Jkb.
Subgroups and minor antigens are also determined in immunohematological studies: A-1, A-2, D, Cc, E, Kell, Duffy.
In patients with sickle cell disease, to reduce the risk of alloimmunization during transfusions, leukocyte-depleted erythrocyte suspension is required, compatible for ABO, Rh, Kell antigen, and rare/minor antigens, with a full expanded erythrocyte phenotype and genotype.
How is laboratory determination of the AB0 blood group performed?
Laboratory determination of the AB0 blood group is carried out by the agglutination reaction method using monoclonal antibodies (soclones) or standard isohemagglutinating sera. A large drop of soclone (anti-A, anti-B, or combined anti-AB) is applied to a plate, after which a 10 times smaller drop of the test blood is added. When an antibody meets an antigen, an agglutination reaction occurs—visible clumps of erythrocytes appear.
| Agglutination with soclones | Antigens present | Blood group |
|---|---|---|
| No agglutination with anti-A and anti-B | No A and B | I (0) |
| Anti-A (+), anti-AB (+) | Antigen A | II (A) |
| Anti-B (+) | Antigen B | III (B) |
| Anti-A (+), anti-B (+) | Antigens A and B | IV (AB) |
What is the pathogenesis of Rhesus conflict during pregnancy?
The pathogenesis of Rhesus conflict is based on incompatibility: the mother is Rhesus-negative, the fetus is Rhesus-positive. During pregnancy, a minimal amount of fetal erythrocytes enters the maternal bloodstream; during childbirth, fetomaternal transfusion of up to 3–4 ml of fetal blood containing the Rhesus antigen occurs. The mother's immune system recognizes the fetal Rh antigen as foreign, isoimmunization (sensitization) develops, and specific anti-Rh/Rhesus antibodies are produced.
In a subsequent pregnancy with a Rhesus-positive fetus, maternal anti-Rhesus IgG antibodies are able to cross the placental barrier. They attack the fetal erythrocytes, causing their hemolysis. The consequences can be hemolytic disease of the newborn, hemolytic jaundice, and severe anemia.
To remember the universal donor and recipient: group 0 (I) is "zero antigens" (will not harm anyone, donated to everyone), and group AB (IV) is "absolutely without antibodies" (no one will attack, accepted from everyone).
What else to study on this topic
- Structure and synthesis of membrane oligosaccharides
- Genetics of AB0 system inheritance
- Characteristics and antigenic composition of the Rhesus system
- Mechanisms of hemolysis in erythrocyte agglutination
- Rules for massive blood transfusion
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