Karl Landsteiner discovered the ABO blood group system in 1901. His work showed that individuals have antigens on their red blood cells and antibodies in their plasma, according to Landsteiner's law. The ABO blood group is determined by the presence or absence of A and B antigens on red blood cells, which is controlled by inherited genes. People are type A, B, AB, or O. The H antigen precursor is present in all groups and is modified by enzymes coded by the A and B genes to produce the A and B antigens. Rare Bombay phenotype individuals lack the H antigen and must receive blood from other Bombay donors.

2. History - Karl
Landsteiner
 Discovered the ABO Blood
Group System in 1901
 He and his five co-workers
began mixing each others red
cells and serum together and
inadvertently performed the
first forward and reverse ABO
groupings

3. Landsteiners
Rule
Karl Landsteiner’s law :
If an antigen is present in the RBC’s of an
individual, the corresponding antibody
must be absent from the plasma
If an antigen is absent in the RBC’s of an
individual, the corresponding antibody
must be present from the plasma

4. MajorABO
BloodGroup
ABO
Group
Antigen
Present
Antigen
Missing
Antibody
Present
A A B Anti-B
B B A Anti-A
O None A and B Anti-A&B
AB A and B None None

5. ABO Basics
Blood group antigens are actually sugars
attached to the red blood cell.
Antigens are “built” onto the red cell.
Individuals inherit a gene which codes for
specific sugar(s) to be added to the red
cell.
The type of sugar added determines the
blood group

6. Principle of
blood
grouping
There are two principles
1-almost all normal healthy individuals above 3-6
months of age have “ naturally occurring Abs” to
the ABO Ags that they lack
These Abs termed naturally occurring because they
were thought to arise without antigenic stimulation

7. Principle of
blood grouping
2- These “naturally occurring” Abs are mostly IgM
class. That means that, they are Abs capable of
agglutinating saline/ low protein suspended red
cell without enhancement and may activate
complement cascade.

8. ABO and H
Antigen
Genetics
O gene on
chromosome
19
 Ags belonging to ABH blood group system are
present on RBCs and other body cells and body
fluids.
 The presence of A,B, and O Ags on RBCs depends
upon the allelic genes, A,B, and O
 An H genes at a separate locus codes for the
precursor substance on which the A and B gene
products act
 The products of the A and B genes are enzymes that
act as a specific transferases

9. Genetics
 The ABO genes do not code for the production of
ABO antigens, BUT rather produce specific fucosyl
transferases
 ABO produces a specific fucosyl transferases that
add sugars to a basic precursor substance on the
RBCs

10. RBC Precursor
Structure Glucose
Galactose
N-acetylglucosamine
Galactose
Precursor
Substance
(stays the
same)
RBC

11. There are two potential precursors substance (PS)
both are comprised of identical sugar (galactose-
N- acetylglucoseamine - galactose -glucose) but
different in linkage.
 Type I PS has a terminal galactose (Gal) linked to a
subterminal N acetylglucoseamine (GlcNAc) in 1-3
linkage
 Type II PS, has the same sugar combine in 1-4
linkage
 ABH Ags on RBCs are derived from Type II chains

12. HAntigen
 The inheritance of at least one H gene (HH or Hh)
elicits (obtain) the production of an enzyme called,
α-2-L-Fucosyl transferase, which transfers the
sugar from the Guanosine diphosphate L-fucose
(GDP-Fuc) donor nucleotide to the terminal
galactose of the precursor chain.
 The H substance must be formed for the other
sugars to be attached in response to an inherited A
and /or B genes

13. Formation of
the H antigen Glucose
Galactose
N-acetylglucosamine
Galactose
Precursor
Substance
(stays the
same)
RBC
H antigen
Fucose

14. A and B
Antigen
 The “A” gene codes for an enzyme (transferase) that
adds N-acetylgalactosamine to the terminal sugar of
the H antigen
 N-acetylgalactosaminyltransferase
 The “B” gene codes for an enzyme that adds D-
galactose to the terminal sugar of the H antigen
 D-galactosyltransferase

15. Formation of
theA antigen Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose
N-acetylgalactosamine
A antigen

16. Formation of
the B antigen Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose
Galactose B antigen

17. Formation of
theAB antigen
Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose
Galactose B antigen
N-acetylgalactosamine A antigen

18. Formation of
the H antigen Glucose
Galactose
N-acetylglucosamine
Galactose
Precursor
Substance
(stays the
same)
RBC
H antigen
Fucose
O antigen

19. Genetics
 The H antigen is found on the RBC when you have the
Hh or HH genotype, but NOT from the hh genotype
 The A antigen is found on the RBC when you have the
Hh, HH, and A/A, A/O, or A/B genotypes
 The B antigen is found on the RBC when you have the
Hh, HH, and B/B, B/O, orA/B genotypes

20. Bombay
Phenotype
(Oh)
 Inheritance of hh
 The h gene is an amorph and results in little or no
production of L-fucosyltransferase
 Originally found in Bombay
 Very rare (130 worldwide)

21. Bombay
Phenotype
(Oh)
 The hh causes NO H antigen to be produced
 Results in RBCs with no H, A, or B antigen (patient
types as O)
 Bombay RBCs are NOT agglutinated with anti-A, anti-
B, or anti-H (no antigens present)
 Bombay serum has strong anti-A, anti-B and anti-H,
agglutinating ALL ABO blood groups
 What bloodABO blood group would you use to
transfuse this patient??
Another Bombay
Group O RBCs cannot be given because they still
have the H antigen
You have to transfuse the patient with blood that
contains NO H antigen

22. Thank you….