BLOOD GROUPS

Mansyur Arif
Bag. Patologi Klinik FK UNHAS / RSUP
Dr. Wahidin Sudirohusodo

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Definitions
Blood groups are determined by antigens
structures on the surfaces or red cells and
are detected by reactions with specific
antibodies.
A blood group system is defined by a.g that
are regulated either by allelic genes or
closely linked genes.

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Antibodies : sources & properties

1. Normal humans
A.bodies to some blood group a.g occur in
the serum of individuals who lack the a.g
and have had no prior exposure to it 
natural isohemagglutins.
The major ones are directed against surface
a.g such as the ABO, Ii and P systems 
controlled by oligosaccharides

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Isohemagglutins with ABO are always clinical-
ly significant
Isohemagglutins  elicited by similar
sequences on microbial surfaces  >>Ig Ms
 effective hemolysins because they
efficiently fix complement)
Occasionally Ig G a.bodies specific for these
a.g also appear.

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2. Immunized animals

If animals are immunized with human red cells

 may form a.bodies to certain of the
xenogeneic blood group a.g  important
source of blood group anti sera  carefully
absorbed with human red cells to establish
specificity.
Recently developed a.g specific monoclonal
a.bodies  do not require such absorption.

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3. Immunized humans

The third major source of the blood group anti

bodies are donors who have been allogenically
immunized either by (1) prior blood
transfusions or (2) previous pregnancies 
immune antibodies  elicited by prior
exposure to red cell a.g are commonly IgGs

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 Methods of detection
1. Agglutination by specific antibody
Under physiologic conditions of pH and ionic
strength, normal red cells repel each other
owing to their negative surface charge or
zeta potential
2. Enhancement of agglutination by antibody
a. Reduction of zeta potential
Can be reduced by addition of colloid (alb,
polyvinylpyrrolidone or dextra).
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 b. Insertion of a.b rd cells bridges
Agglutinations may produced or enhanced
by addition of Coomb reagent (i.e.,anti-
globulin a.body)
3. Use of lectins
4. Automated techniques

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 Genetics
• According to mendelian laws
• Heredity is generally autosomal
codominant i.e there is an expression of
both alleles in the heterozygous individual
1. Linked genes
2. Interaction with other genes
3. Loci of blood groups genes on
chromosomes
4. Occurrence of blood group antigens
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 ABO SYSTEM
a. Historical notes
In subsequent work Landsteiner recognized
that the pattern of reactions could be
explained by two a.g, which designated A
and B. O signified the state of not having A
or B.
Table 1. The Landsteiner scheme

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Table 1. The ABO system defined by Anti-A and Anti B

Blood Groups Antigens on RC Antibodies in serum

O None Anti-A and Anti-B
A A Anti-B
B B Anti-A
AB A and B None

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b. Subdivisions of A antigen

A antigen and anti-A are complex. Anti-A

serum from a group B donor contains 2 types
of a.b, anti-A and anti-A1 . (table 2)

Group Antigens Reaction with

Anti-A Anti-A1
A1 AA1 + +
A2 A + -

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Genetics
Determining the blood group : genotype and
phenotype. A child receives one of four genes
from each parent : A1, A2, B1, or O. Six
phenotypes are possible because the A a.g
associated with group A2 and also A1.
There are ten possible genotypes. Group A1 may
have 3 genotypes (A1 A1, A2 O, A1A2). Group A2
can have either A2A2 or A2 O genotypes. Group
B can have either BB or BO genotypes
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• Genotype :
- specific genes that person carries
- determined by family studies
- AA, AO, BB, BO, AB and OO
- see fig 1.

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 Family 1

Phenotype B A1
Genotype BO A1O

Phenotype O O A1B
Genotype OO OO A1B

Family 2

Phenotype A1 A2B
Genotype A1A2 A2B

Phenotype A2B A1
Genotype A2B A1A2

Fig 1. Illustration of usefulness of family studies in the elucidation of phenotype

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Phenotype :
Four phenotypes : A, B, AB and O
Although there are ten possible genotypes,
the absence of a specific anti-O prevents the
serological recognition of more than four
phenotypes. (table 2)

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Table 2. Blood Type

Phenotype Genotype Antigens Antibodies in

on red cell plasma

O OO O Anti-A, Anti-B
A AA or AO A Anti-B
B BB or BO B Anti-A
AB AB AB None

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Fig.2 Synthesis of ABH antigens
R

glc gal glcnac gal

H precursor
Hh gen

fuc
R

glc gal glcnac gal H antigen

A gene B gene

fuc fuc
R R

glc gal glcnac gal glcnac glc gal glcnac gal gal
A antigen B antigen
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 H antigen

• The surfaces oligosaccharides that constitutes

the H a.g is the precursor of the A and B a.g

• Gene A & B responsible for converting H

substance into A & B substance

• Gene O has no effects on H substance

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Rare variant  Bombay, the H precursor
cannot be converted to H  lack H ag &
hence A or B phenotype can’t be expressed.
A terminal sugar molecules determine a.g
specificity :
– A a.g : N acetylgalactosamine
– B a.g : galactosa

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 Rhesus System
Rhesus a.b  >> immune (previous transfusion or
pregnancy), naturally <<
Nomenclature : relation to genetic models
1. Fischer-Race theory : postulates 3 closely linked
genes Cc, Dd and Ee. Rhesus a.g is renamed D.
– Rhesus positive  presence of the D antigen,
also called Rh or Rh factor
– Rhesus negative  absence of D but doesn’t
denote absence of other a.g of the Rh system
(C,c,E or e)
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 2. Weiner system
3. Rosenfield system
Compound antigens
Weakened antigens :
- weakly reactive ag  Du
- formal terminology : Rh +, Du variant
- for transfusion : Du is equivalent to Rh +
Deleted antigens : Rh null cells.
Rh antigens structure

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Uses of blood grouping data

A. In clinical medicine
1.Pretransfusion testing :
Prior to transfusion, bllod is typed
and crossmatched to establish
ABO and D compatibility
2.Hemolytic disease of the newborn

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B. In genetics  chromosome mapping
C. In forensic medicine
1. Identification studies
2. Paternity testing

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 Terima kasih

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