NCERT grounding
NCERT Class XI Biology, Chapter 15 — Body Fluids and Circulation, section 15.1.3 Blood Groups — opens by noting that although human blood looks similar from person to person, it differs at the molecular level, and that two grouping systems — the ABO and the Rh — are used worldwide. Section 15.1.3.1 fixes the ABO system on two surface antigens (A and B) of the RBC and two natural plasma antibodies (anti-A and anti-B). Section 15.1.3.2 introduces the Rh antigen, named after the rhesus monkey, present in roughly 80 per cent of humans, and sets up the special case of Rh incompatibility between an Rh-negative mother and her Rh-positive foetus.
"ABO grouping is based on the presence or absence of two surface antigens on the RBCs namely A and B. The plasma of different individuals contain two natural antibodies."
NCERT XI · Biology · §15.1.3
The ABO system in depth
The ABO system was discovered by the Austrian immunologist Karl Landsteiner in 1900 — work that earned him the 1930 Nobel Prize in Physiology or Medicine. Landsteiner mixed red cells from one person with plasma from another and noticed that some combinations triggered agglutination — clumping of red cells — while others did not. The pattern of clumping mapped onto two surface molecules on the RBC, which he named antigen A and antigen B, and two corresponding natural plasma antibodies, anti-A and anti-B.
An antigen is a chemical (here, an oligosaccharide on a glycolipid anchored in the RBC plasma membrane) capable of inducing an immune response. An antibody is a protein produced in response to an antigen. The ABO antibodies are unusual in being naturally present from infancy without prior exposure to foreign blood — they appear because gut bacteria carry similar sugar structures that prime the immune system early in life. The cardinal rule of the ABO system is simple and absolute: a person cannot carry, in plasma, the antibody against an antigen present on his or her own RBCs. If they did, their own red cells would be destroyed.
ABO phenotypes
A, B, AB and O — defined by which combination of A and B antigens sits on the red cell surface, and (by the cardinal rule) which anti-A or anti-B antibody is present in plasma.
The four ABO phenotypes
Three alleles at the ABO locus determine the phenotype: IA, IB and i. IA and IB are co-dominant — both express in an AB heterozygote — while i is recessive and codes for no antigen. The genotype-to-phenotype mapping is therefore: IAIA or IAi → A; IBIB or IBi → B; IAIB → AB; ii → O.
| Blood group | Antigens on RBC | Antibodies in plasma | Possible genotypes |
|---|---|---|---|
| A | A | anti-B | IAIA, IAi |
| B | B | anti-A | IBIB, IBi |
| AB | A and B | nil | IAIB |
| O | nil | anti-A and anti-B | ii |
Read the table along the cardinal rule. Group A has antigen A on its red cells and therefore cannot have anti-A in plasma — but it freely carries anti-B. Group B mirrors this. Group AB carries both antigens, so neither anti-A nor anti-B can survive in its plasma. Group O carries neither antigen, so both anti-A and anti-B circulate freely.
Figure 1. The four ABO groups. Antigens A and B sit on the red cell surface; the matching antibody is always absent from the same individual's plasma, and the unmatched antibodies are present.
Donor–recipient compatibility
During a transfusion, what matters is whether the recipient's plasma antibodies will attack the donor's red cells. (Donor plasma is usually small in volume and gets diluted, so the more important interaction is recipient-antibody vs donor-antigen.) Wherever a recipient antibody meets a corresponding donor antigen on the RBC surface, agglutination occurs — the foreign red cells clump, block capillaries and rupture, releasing haemoglobin (haemolysis). A mismatched transfusion can therefore be rapidly fatal.
| Recipient ↓ / Donor → | O | A | B | AB |
|---|---|---|---|---|
| O (anti-A, anti-B) | ✓ | ✗ | ✗ | ✗ |
| A (anti-B) | ✓ | ✓ | ✗ | ✗ |
| B (anti-A) | ✓ | ✗ | ✓ | ✗ |
| AB (no antibodies) | ✓ | ✓ | ✓ | ✓ |
Read along each row: AB receives from everyone because it carries no anti-A and no anti-B; O receives only from O because its plasma carries both antibodies. Read down each column: O donates to everyone because its red cells carry no A and no B antigen for any recipient antibody to attack; AB donates only to AB.
Group O — Universal donor
O
no A, no B antigen on RBCs
- Donor RBCs carry neither antigen, so recipient anti-A and anti-B have nothing to bind.
- Plasma of the O donor carries both anti-A and anti-B (so O donors cannot be universal recipients).
- In practice, the safest universal-donor preparation is packed red cells (plasma removed).
Group AB — Universal recipient
AB
no anti-A, no anti-B in plasma
- Recipient plasma contains no ABO antibodies, so donor RBCs of any ABO group are not agglutinated.
- RBCs of the AB recipient still carry both antigens, so AB can donate only to AB.
- Rh status must still be matched — AB+ can receive Rh+ or Rh− blood; AB− should not receive Rh+ blood.
The Rh system
The Rh blood group system is a second, independent surface-antigen classification of human RBCs, discovered in 1940 by Landsteiner together with Alexander Wiener. The antigen they identified on human cells turned out to be similar to one previously found on the red cells of the rhesus monkey (Macaca mulatta), giving rise to the abbreviation Rh. Roughly 80 per cent of humans express the Rh antigen on their RBCs and are termed Rh positive (Rh+); those who lack it are Rh negative (Rh−).
Rh positive
Carry the Rh antigen on RBCs; can receive both Rh+ and Rh− blood.
Rh negative
Lack the Rh antigen; can develop anti-Rh antibodies on exposure to Rh+ blood and must therefore receive only Rh− blood.
The Rh system differs from ABO in one crucial respect: anti-Rh antibodies are not naturally present in Rh− plasma. They appear only after an Rh− individual is exposed to Rh+ red cells — through transfusion or, more commonly, through pregnancy. Once those antibodies are formed, a subsequent exposure to Rh+ blood will trigger an immune attack on the foreign red cells. Therefore, Rh group must be matched alongside the ABO group before any transfusion.
Erythroblastosis foetalis
The clinically important consequence of Rh incompatibility occurs in pregnancy. If an Rh− mother carries an Rh+ foetus (the father being Rh+), the placenta normally keeps the two bloods well separated, and the first pregnancy usually proceeds without harm. However, at the time of delivery, small amounts of foetal Rh+ blood inevitably leak into the maternal circulation. The mother's immune system then mounts a response and begins to manufacture anti-Rh antibodies — a process called sensitisation.
Because IgG-class anti-Rh antibodies can cross the placenta, a subsequent Rh+ pregnancy is in danger. Maternal anti-Rh antibodies leak across the placenta into the foetal circulation and bind to the Rh antigens on foetal RBCs. The coated red cells are destroyed in large numbers — a haemolytic disease of the newborn known as erythroblastosis foetalis (so named because immature, nucleated red cells called erythroblasts spill into the foetal blood as the bone marrow tries to compensate). The baby may show severe anaemia, jaundice, enlarged liver and spleen, and in untreated cases the condition can be fatal.
Sensitisation and erythroblastosis foetalis — the four steps
-
Step 1
First pregnancy
Placenta keeps maternal and foetal blood separated; no exposure during gestation, baby is safe.
-
Step 2
Delivery
Small amounts of Rh+ foetal blood enter maternal circulation as the placenta detaches.
-
Step 3
Sensitisation
Mother's immune system makes anti-Rh antibodies (IgG) against the foetal Rh antigen.
-
Step 4
Next Rh+ pregnancy
Maternal anti-Rh IgG crosses placenta, destroys foetal RBCs → erythroblastosis foetalis.
Prevention — anti-Rh (RhoGAM)
The disease can be prevented by giving the Rh− mother anti-Rh antibodies — commercially known as RhoGAM or anti-D immunoglobulin — within 72 hours of the delivery of the first Rh+ child, and after any event during pregnancy that could expose her to foetal blood (amniocentesis, abortion, abdominal trauma). The injected antibodies bind to and clear the foetal Rh+ cells from her circulation before her own immune system can recognise the Rh antigen and produce a memory response. Because she never becomes sensitised, future Rh+ pregnancies are protected.
Figure 2. The first Rh+ pregnancy is normally safe because the placenta separates the two bloods. Sensitisation at delivery generates maternal anti-Rh IgG, which crosses the placenta in any subsequent Rh+ pregnancy and lyses foetal red cells. Prevention is by administering anti-Rh (RhoGAM) to the mother immediately after the first delivery.
Blood-bank significance
Blood banks routinely test every donation and every patient sample for both the ABO and the Rh systems before any transfusion is released. The clinical workflow rests on three precautions. Cross-matching is performed in vitro — donor RBCs are mixed with recipient plasma and observed for agglutination. Both ABO and Rh must match: an Rh− recipient who has previously been exposed to Rh+ blood carries anti-Rh antibodies that can lyse Rh+ donor cells. Rh− blood is precious in inventory terms because Rh− recipients (about a fifth of the population) can only receive Rh− blood; Rh+ recipients can receive either.
Worked examples
A patient with blood group A needs a transfusion. From which ABO groups can blood be safely accepted?
Solution. A patient with group A carries antigen A on RBCs and anti-B in plasma. Donor RBCs must not carry antigen B (else the recipient's anti-B will agglutinate them). Hence the only safe donors are group A (carries only antigen A) and group O (no antigen). B and AB are unsafe.
An Rh− woman had a normal first pregnancy with an Rh+ baby. She did not receive RhoGAM. Why is her second Rh+ pregnancy at risk?
Solution. Exposure to foetal Rh+ blood at the first delivery sensitises her immune system. She produces anti-Rh IgG antibodies, which are now present in her plasma. In any subsequent Rh+ pregnancy, this IgG crosses the placenta and binds to foetal Rh+ RBCs, leading to their destruction — erythroblastosis foetalis. RhoGAM after the first delivery would have cleared the foetal cells before her immune system mounted a memory response.
A father is B+ and the mother is A+. They have a child who is O+. Give one possible genotype for each.
Solution. The O child must be ii, so each parent must carry one recessive i allele. The father (B phenotype, carrying an i allele) must therefore be IBi, and the mother (A phenotype, carrying an i allele) must be IAi. Genotypes: father IBi, mother IAi, child ii. The cross IBi × IAi predicts AB, A, B and O children in equal ratio. The Rh+ child only requires that one of the parents carries at least one dominant Rh allele.