BACHELOR OF BIOMEDICAL SCIENCES

BASIC TRANSFUSION SCIENCE AND BLOOD BANKING

BMC 125

CHAPTER 5: OTHER BLOOD GROUPING SYSTEM

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 Learning Outcomes :
At the end of the lecture, students should be able to:
• Describe the various blood group systems including :
(1)Lewis system
(2)Ii system
(3)P system
(4)MNSs system
(5)Kell
(6)Kidd
(7)Duffy
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 Introduction

• Approximately 300 red blood cell antigens with 30

different blood group system discovered and registered
with International Society of Blood Transfusion (ISBT).
• We will discuss each of these major antigens, their
antibodies, and the clinical significance of each.

• Generally other blood groups system divided into

1. common other blood groups systems.
2. uncommon other blood group systems.

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 Common Other Blood Group Systems

• Lewis
• Ii
• P
• MNSs
• Kell
• Kidd
• Duffy
• Diego
• Lutheran
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 Uncommon Other Blood Group System
• Gerbich
• Xg
• Scianna
• Cartwright
• Dombrock
• Cromer
• Colton
• Chido/Rodgers
• JMH
• OK
• RAPH
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 Basic terms to remember
• Clinical significance antibodies: antibodies that are
associated with decreased RBC survival
– Transfusion reactions
– HDN
• Not clinically significant antibodies: antibodies that
do not cause red cell destruction
• Cold reacting antibodies: agglutination best
observed at or below room temp.
• Warm reacting antibodies: agglutination best
observed at 37°C

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Systems that Produce Cold-Reacting
Antibodies

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 LEWIS SYSTEM
Lewis Antigens
• 2 main antigens : Lea (1946) and Leb (1948).
• Soluble antigens are produced by tissues and
found in body fluids (plasma). Lewis substance
adheres to RBC
• Adsorbed on the RBC becoming an antigen

RBC

Le substance
in plasma
Le
genes
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 Lewis inheritance
• Lewis system depends on Le, Se and H genes
• le, se and hh do not produce products
• If the Le gene is inherited, Lea substance is produced
• Le, Se and Hh genes must ALL be inherited to
convert Lea to Leb. Examples:

– Le se Hh  Le(a+b-)
– Le Se Hh Le(a-b+)
– le se Hh  Le(a-b-)

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 Lewis Antibodies

• IgM in nature and may react strongly at RT (may fix

complement, becoming hemolytic in vitro)
• Lewis antibodies occur almost exclusively in the sera
of Le(a-b-) persons.
• No clinical significance…Why?
– Because Lewis antibodies do not cross placenta and
the antibodies have not been implicated in HDN.

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 I SYSTEM
I antigens
• These antigens may be I or i
• Fetal RBCs are rich in ‘i’ antigen, and lack I antigen.
• During the first 2 years of life, the I antigen
gradually develops, and there is a concomitant loss
of ‘i’ antigen.
• Adults have I antigen – almost everyone
• Thus the RBCs of most adults react strongly with
anti-I while baby cells non-reactive with anti-I.

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 I antibodies

• Most people have autoantibody -I (RT or 4°C)

• Alloantibody -I is very rare
• Cold-reacting (RT or below) IgM antibody
• Clinically insignificant (IgM doesn't cause
HDN)
• Enzymes can enhance detection

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 Anti-I antibodies
• Anti-I:
– Associated as a cause of Cold Agglutinin Disease
may be secondary to Mycoplasma pneumoniae
infections
• Anti-i:
– rare and is sometimes associated with infectious
mononucleosis caused by the Epstein-Barr virus
and cytomegalovirus(CMV)

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 P SYSTEM
P Antigen

• Similar to the ABO system

• The most common phenotypes are P1 and P2
– P1 – consists of P1 and P antigens
– P2 – consists of only P antigens
• Like the A2 subgroup, P2 groups can produce anti-P1
• 75% of adults have P1

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 P antibodies
• Anti-P1
– Naturally occurring IgM
– Not clinically significant
• Anti-P
– Produced in individuals with paroxysmal cold
haemoglobinuria (PCH)
– PCH – IgG auto-anti-P attaches complement when
exposure to cold (fingers, toes). As the red cells
circulate, they begin to lyse (releasing Hb)
– This PCH antibody is also called the Donath-Landsteiner
antibody
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 MNSs Blood System
• 4 important antigens (more exist):
–M
–N
–S
–s
– U (ALWAYS present when S & s are inherited)
• M & N located on Glycophorin A
• S & s and U located on Glycophorin B
• Remember: Glycophorin is a protein that carries
many RBC antigens
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 MNSs Antigens

M & N only differ in

M their amino acid
Glycophorin A N sequence at positions
1 and 5

RBC

S S & s only differ in

U
Glycophorin B
s their amino acid
sequence at position
29

COOH end ….. ….5, 4, 3, 2, 1 (NH2 end)

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 MNSs antigens
• M & N give a stronger reaction when
homozygous, (M+N-) or (M-N+)
• Weaker reactions occur when in the
heterozygous state (M+N+)
• Antigens are destroyed by enzymes (i.e. ficin,
papain)

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 Anti-M and anti-N antibodies
• Anti-M are predominantly IgM (rarely IgG)
– Clinically insignificant
– If IgG, could be implicated in HDN (RARE)

• Anti-N are comparatively rare, IgM

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 Anti-S, Anti-s, and Anti-U

• Clinically significant
• IgG
• Can cause RBC destruction and HDN

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 MNSs Antibody Characteristics
Antibody IgG Class Clinically
significant
Anti-M IgM (rare IgG) No

Anti-N IgM No

Anti-S IgG Yes

Anti-s IgG Yes

Anti-U IgG Yes

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Systems that Produce Warm-Reacting
Antibodies

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 Kell System

• Similar to the Rh system

• 2 major antigens
– K (Kell)
– k (cellano)
• Well developed at birth
• The K antigen is very immunogenic (2nd to the D
antigen) in stimulating antibody production
• 90% of populations are ‘K’ negative (K-k+); (K+,k-
0.2%) (K+k+ 8%)
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 Other Kell antigens
• Other sets of alleles also exist in the Kell
system:
• Kp antigens
– Kpa is a low frequency antigen (only 2%)
– Kpb is a high frequency antigen (99.9%)
• Js antigens
– Jsa (20% in Blacks, 0.1% in Whites)
– Jsb is high frequency (80-100%)

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 Kell antibodies
IgG (react well at AHG)
Produced as a result of immune stimulation
(transfusion, pregnancy)
Clinically significant
Anti-K is most common because the K antigen is
extremely immunogenic (90% of donors are K negative)
k, Kpb, and Jsb antibodies are rare (many individuals have
these antigens and won’t develop an antibody)
The other antibodies are also rare since few donors have
the antigen
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 Kidd Blood Group System
• 2 antigens
– Jka and Jkb

Genotype Phenotype Whites (%) Blacks (%)

JkaJka Jk(a+b-) 26.3 51.1
JkaJkb Jk( a+b+) 50.3 40.8
JkbJkb Jk(a-b+) 23.4 8.1
JkJk Jk(a-b-) rare rare

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 Kidd Antigens
• Well developed at birth
• Enhanced by enzymes

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 Kidd antibodies
• Anti-Jka and Anti-Jkb
– IgG
– Clinically significant
– Implicated in HTR and HDN
– Common cause of delayed HTR

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 Duffy Blood Group System
– Fya and Fyb code for antigens that are well developed at
birth
– Antigens are destroyed by enzymes, so will give
negative reactions in enzyme test procedure

Duffy antibodies:
– IgG
– Do not bind complement
– Clinically significant
– Stimulated by transfusion or pregnancy (but not a
common cause of HDN)
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Other Blood Group Antigens…

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 Lutheran Blood Group System
• Antigen: Lua and Lub
• Most individuals (92%) have the Lub antigen

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 Lutheran antibodies

• Anti- Lua
– IgM and IgG
– Poorly developed at birth, Anti- Lua has not been reported to
cause HDN
– Has not been associated with HTRs
– Not clinically significant
– Naturally occurring or immune stimulated and reacts at room
temperature
• Anti- Lub
– IgG type, rare because Lub is high incidence antigen
– Associated with transfusion reactions (rare HDN)

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 Bg Antigens
• Three (Bennett- Goodspeed) Bg antigens:
• Bg antigens are expressed to variable degrees on RBCs
– Bga
– Bgb
– Bgc

Sda Antigens
• High incidence antigens found in tissues and body fluids
• Antigen is variably expressed on the cells
• Antibodies are not clinically significant
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 Cold Antibodies (IgM)
Anti-Lea
Anti-Leb
Anti-I
Anti-P1
Anti-M
Anti-A, -B, -H
Anti-N

LIiPMABHN
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Warm antibodies (IgG)

• Rh antibodies
• Kell
• Duffy
• Kidd
• S,s

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 REFERENCES
• Denise M. Harmening PhD MLS(ASCP)
CLS(NCA),2012.Modern Blood Banking &
Transfusion Practices 6th Edition.by F.A.Davis
company united sate of America.
• Eva D.Quinley Ms MT
(ASCP)SBB.2010.immunohaematology Principles and
practice,3rd ed( Lippincott Williams and Wikins)
• Jeffrey Mc Cullough.2011.Trnasfusion Medicine 3 rd
ed,wiley Blackwell publication ,United states.
• Harvey G.Klein,David J Anstee 2013,Mollisons blood
transfusion in clinical medicine,12 th ed,Wiley-Blackwell.
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Thank you

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