The document summarizes key information about major blood group systems including ABO, Rh, Lewis, Kell, Duffy, and Kidd. It describes the antigens and genes involved in determining blood group types, frequencies in different populations, clinically significant antibodies, and associations with diseases.

1. Dr. Nawsherwan Sadiq
Department of
Pathology/Haematology
Hawler Medical University
College of Medicine

2. ABO SYSTEM
• There are four main blood groups: A, B, AB
and O.
• In the British Caucasian population, the
frequency of group A is 42%, B 9%, AB 3%, and
O 46%
• there is racial variation in these frequencies.[6]
The epitopes of ABO antigens are determined
by carbohydrates (sugars), which are linked
either to polypeptides (forming glycoproteins)
or to lipids (glycolipids).

3. In Caucasians the most frequent
ABO phenotype is the O followed
by A, B and least is AB.
Three genes on Chromosome 9
determine the ABO phenotype
namely A, B and O gene.

4. • The A and B genes do not code for A or B
antigens, but they code for specific enzymes
“Glycosyl transferases” which add sugars to
a basic precursor substance.
• The expression of the A and B antigens
requires the presence of an independently
inherited H gene.

5. • The immunodominant sugar added to
produce the
• A antigen is : N-acetylgalactoseamine
• B antigen is : D-galactose
• H antigen is : L-Fucose.

6. Enzymes are:
• A antigen : α-3-N-acetylgalactosaminyl
transferase.
• B Antigen :α-3-D-galactosyl transferase
• H antigen : α-2-L-fucosyl transferase.

8. Frequency of Blood Groups in the General Population
Blood Groups Frequency (%)
Type
O 47
A 41
B 9
AB 3
Rh factor
Rh - 15
Rh + 85
From Guyton AC: Textbook of Medical Physiology, 6th ed. Philadelphia, WB
Saunders, 1981.

10. In the extremely rare Oh Bombay phenotype, the
individual is homozygous for the h allele of FUT1
and hence cannot form the H precursor of the A
and B antigen.
Their red cells type as group O, but their plasma
contains anti-H, in addition to anti-A, anti-B, and
anti-A,B, which are all active at 37°C.
As a consequence, individuals with an Oh Bombay
phenotype can only be safely transfused with other
Oh red cells

11. • Subjects with H Antigen should either be
HH or Hh,
• if he/she is hh, then no L-Fucose is added, so
no H, A or B antigens could be produced.
called Bombay blood Group.
• The H gene is seen in 99.99% of subjects
(either Hh, or HH),
• the hh is very rare seen in 0.01%.

12. • Two common subgroups of the A antigen.
Approximately 20% of group A and group AB
individuals belong to group A2 and group A2B.
• The remainder belonging to group A1 and
group A1B.
• These subgroups arise as a result of
inheritance of either the A1 or A2 alleles.

13. • A2 red cells have fewer A antigen sites than A1
cells and the plasma of group A2 and group A2B
individuals may also contain anti-A1.
• The distinction between these subgroups can
be made using the lectin Dolichos biflorus,
which only reacts with A1 cells

14. • The H antigen content of red cells depends on
the ABO group.
• The strength of reaction tends to be graded O
> A2 > A2B > B > A1 > A1B.
• Other subgroups of A are occasionally found
(e.g., A3, Ax) that result from mutant forms of
the glycosyltransferases produced by the A
gene

15. • A phenotype : the Genotype maybe either
AA or AO.
• B phenotype : The Genotype maybe either
BB or BO.
• AB phenotype : The Genotype is AB.
• O phenotype : The Genotype is OO.

16. • ABH antigens develop as early as 37 days
fetal life.
Weakly expressed throughout fetal life.
• In newborn the ABO Ag sites are about 25-
50% strength of those in adults.
• The number of antigen sites reaches “adult”
level at around 1 year of age and remains
constant until old age, when a slight
reduction may occur..

17. Secretors and Nonsecretors
• The ability to secrete A, B, and H substances in
water-soluble form is controlled by FUT2
(dominant allele Se).
• In a Caucasian population, about 80% are
secretors (genotype SeSe or Sese) and 20% are
nonsecretors (genotype sese).
• Secretors have H substance in the saliva and
other body fluids together with A substances,
B substances, or both, depending on their
blood group.

18. • Only traces of these substances are present in
the secretions of nonsecretors, although the
antigens are expressed normally on their red
cells and other tissues.
• An individual's secretor status can be
determined by testing for ABH substance in
saliva

19. ABO Antigens and Disease
• Group A individuals rarely may acquire a B
antigen from a bacterial infection that results
in the release of a deacetylase enzyme.
• This converts N-acetyl-D-galactosamine into
α-galactosamine, which is similar to galactose,
the immunodominant sugar of group B.
• Thereby sometimes causing the red cells to
appear to be group AB.

20. • Case reports attest to the danger of
individuals with an acquired B antigen being
transfused with AB red cells, resulting in a
fatal haemolytic transfusion reaction following
the production of hyperimmune anti-B.

21. • Group A individuals have 1.2 times the risk of
developing carcinoma of the stomach than
group O or B;
• Group O individuals have 1.4 times more risk
of developing peptic ulcer than non-group O
individuals.
• Nonsecretors of ABH have 1.5 times the risk of
developing peptic ulcer than secretors.

22. • The ABO group also affects plasma von
Willebrand factor (vWF) and factor VIII levels;
group O healthy individuals have levels
around 25% lower than those of other ABO
groups.
• ABH antigens are also frequently more weakly
expressed on the red cells of persons with
leukaemia.

23. • Regarding the ABO group, all normal
healthy individuals consistently have
present in their sera, antibodies to antigens
they lack on their red cells.
• This is not true regarding other blood
groups.

24. ABO Abs
• Naturally occurring
• Bacteria, pollen seeds, diet, or other substances
present in nature have been implicated in
stimulating Antibody development..
• Starts at first few months after birth.
• Detectable titres of Abs by 3-6 months.
• Peaks at 5-10 yrs.
• Declines progressively with advanced age.
• 0.01% healthy individuals may not have natural
occurring antibodies.

26. Rh System
DECce
• Wiener Rh-Hr terminology shorthand
designation: is among the most commonly
used ones to denote Rh haplotype
• R1 CDe r cde
• R2 cDE r’ Cde
• Ro cDe r” cdE
• Rz CDE ry CdE

27. • In Caucasians :
R1 > r > R2 > Ro > r’ > r”.
• Rhnull is a person who expresses no Rh
Antigens on his red cells (---/---)

28. Weak D or Du
• Maybe detected by some but not all anti-D
reagents or by using IAGT and not directly.

29. • Most are IgG.
• React optimally at 37C.
• They have been significantly linked to
Hemolytic disease of the newborn and
hemolytic transfusion reactions.
• Immunogenecity of the RH Antigens in
order of potency D>c>E>C>e.

30. Lewis
• Lewis antigens are not synthesized by the red cells
• Lewis Antigens are made up by tissue cells and
secreted into the fluids and plasma.
• They are then absorbed onto the RBC membrane.
• Lewis antigens in secretions are glycoproteins, on
cell membranes glycolipids.
• There antibodies are rarely reactive at 37 C,
therefore they are not significant.

31. Kell System
• Found only on RBC
• Well developed at birth.
• It is next to D in immunogenecity.
• Anti-K is an immune IgG antibody
detectable by IAGT .
• Anti-K is implicated in HDN and HTR.

32. Duffy blood group
• Fya and Fyb are well developed at birth .
• Fy (a-b-) prevalent in blacks and linked
with resistance to malaria.
• Anti Fya and Fyb are IgG immune
antibodies.
• They are reactive by IAGT.
• They are important causes of HDN and
HTR.

33. KIDD System
• Jka and Jkb antigens are well developed at
birth.
• Anti Jka and Jkb are immune IgG antibodies.
• These antibodies unlike duffy’s are
enhanced by enzymes.
• Common causes of severe delayed
transfusion reactions and HDN.

34. Other Blood Group systems
• P system
• Lutheran.
• MNSs system.
• Ii system.
• Less important than those before
mentioned.