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Blood Groups

For medical students3 min readUpdated 2026-10-10

Blood group specificity is determined by the presence of specific glycoproteins (oligosaccharides) on the outer surface of the erythrocyte membrane. In clinical practice, the AB0 and Rhesus (Rh) systems play the primary role, upon which the safety of blood transfusions directly depends.

Molecular basisAntigenic properties depend on the diversity of membrane oligosaccharides.
Main systemAB0 is the most clinically significant blood group system.
Core of conflictAgglutination occurs when corresponding antigens and antibodies meet.
Broad localizationBlood group antigens are present in saliva, tissues, milk, and semen.

General Characteristics and Localization of Antigens

The antigenic properties of blood cells depend on specific chemical structures on their surface. These structures are based on oligosaccharides that form part of the glycoprotein complexes of the outer cell membrane.

In immunohematology, several systems classify blood according to these features, but two are considered fundamental:

It is important to note that blood group antigens are not exclusive to erythrocytes. They are also expressed on platelet membranes, cells of various body tissues, and are even secreted in fluids such as saliva, breast milk, and seminal fluid.

Characteristics of Blood Groups in the AB0 System

The AB0 system is based on the presence of two types of protein structures: antigens (aglutinogens) located on the erythrocyte membrane, and antibodies (agglutinins) circulating in the blood plasma. Depending on their combination, there are four main groups:

  1. Group I (0)

Only the basic 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, found in approximately 40% of people.

  1. Group II (A)

Erythrocytes carry the basic 0 antigen and the A antigen. Only anti-B antibodies are produced in the plasma. This phenotype is the most frequent, covering about 43% of the population.

  1. Group III (B)

Membranes of red blood cells contain 0 and B antigens. The plasma contains anti-A antibodies. This group is less common, carried by approximately 12% of people.

  1. 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 from 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 transfusions. 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 (e.g., antigen A encounters anti-A). In clinical practice, two vectors of immune attack are distinguished:

Principles of Blood Transfusion

When transfusing small volumes of blood, the dilution rule applies: donor antibodies (agglutinins), upon entering the recipient's bloodstream, are diluted multiple times by the recipient's plasma, causing their concentration to drop below a critical level so 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 infused donor erythrocytes.

Basic compatibility rules for small volumes:

Mnemonic

To remember the universal donor and recipient: group 0 (I) is "zero antigens" (harms no one, donated to everyone), and group AB (IV) is "absolutely no antibodies" (no one attacks, received from everyone).

Frequently asked 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. Additional systems/antigens and rare (minor) factors mentioned in sources include:

  • Kell: K, k, Kpa, Kpb.
  • Duffy: Fya, Fyb.
  • Lewis.
  • MNS.
  • Jka, Jkb.

Subgroups and minor antigens such as A-1, A-2, D, Cc, E, Kell, and Duffy are also determined in immunohematological studies.

In patients with sickle cell disease, to reduce the risk of alloimmunization during transfusions, leukocyte-depleted erythrocyte suspension compatible for ABO, Rh, Kell antigen, and rare/minor antigens with a complete extended phenotype and erythrocyte genotype is required.

How is laboratory determination of the AB0 blood group performed?

Laboratory determination of the AB0 blood group is performed using the agglutination reaction method with monoclonal antibodies (zoliclones) or standard isohemagglutinating serums. A large drop of zoliclone (anti-A, anti-B, or combined anti-AB) is placed on a plate, followed by a drop of the test blood that is 10 times smaller. When an antibody meets an antigen, an agglutination reaction occurs — visible clumps of erythrocytes appear.

Agglutination with ZoliclonesPresent AntigensBlood Group
No agglutination with anti-A and anti-BNo A and BI (0)
Anti-A (+), anti-AB (+)Antigen AII (A)
Anti-B (+)Antigen BIII (B)
Anti-A (+), anti-B (+)Antigens A and BIV (AB)
What is the pathogenesis of Rhesus incompatibility during pregnancy?

The pathogenesis of Rhesus incompatibility is based on incompatibility: the mother is Rhesus-negative, and 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, leading to isoimmunization (sensitization) and the production of specific anti-Rh/anti-Rhesus antibodies.

During 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 hemolysis. The consequences can include hemolytic disease of the newborn, hemolytic jaundice, and severe anemia.

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