REVIEW OF IMPORTANT GENETIC

PRINCIPLES AS APPLIED TO BLOOD

BANKING LECTURE 2021 – 2022
Instructor: Joseph Joy Banzon, RMT, MPH 2nd Semester
Date: March 11, 2022 WEEK 4 IMHM321

TOPIC OUTLINE
I. Introduction
II. Blood Group System
III. Other Terminologies in Genetics
IV. Dosage Effects
V. Inheritance Patterns
VI. ABO Blood Group System
VII. ABO Discrepancies
VIII. Frequency Distribution of ABO Phenotypes
IX. ABO Compatibility for Whole Blood, Plasma,
and RBC Transfusion
X. ABO Antibodies

INTRODUCTION

Ø Genetics – it is the study of HEREDITY; transmission of

TRAITS from parents to offspring.
• Blood types are inherited from parents which can
either be the same with the father or mother or a
combination of their genes.
• Blood type is a part of the trait that an individual can Table 1. Blood Group System
inherit from parents. (Kindly, refer to the bigger picture at the last pages)

• List of the first 30 Blood Group System listed by

BLOOD GROUP SYSTEM
International Society of Blood Transfusion (ISBT).
• International Society of Blood Transfusion (ISBT)
Ø Blood Group Systems – group of related red cell – an organization based in US that is responsible for
antigens which is similar in term of biochemical structure, the nomenclature or naming of red cell antigens of
location in RBC, serologic properties and genetic control each blood group system. They also assign 3-digit
of antigen expression. number for every blood group system chronologically.
• There are 36 blood group system that was discovered • Rh Blood System is different to Rh-associated
as of today. glycoprotein.
• Blood type depends on the red cell antigen present in • Part of the table is the Chromosomal Location of the
the red blood cell. genes coding for the production of red cell antigens
• There are a lot of red cell antigens in the body, for every blood group system.
wherein more than 250 red cell antigen were grouped § (e.g. Genes coding for the production of A or B antigens
in 36 blood group system. that will dictate ABO Blood Group System are all
located in Chromosome #9.)
§ Remember, one of the basis in grouping red cell
Ø The basis in grouping Red Cell Antigens is their antigen is they are the same in terms of their genetic
similarities in: control or in chromosomal location.
a. Biochemical Structure (e.g. Rh antigens are made • Even though, red cell antigens have the same
up of pure proteins, making them highly structure or location in RBC, but if they are in different
immunogenic) chromosomal location, they will not be grouped into
b. Location in RBC (e.g. AB antigens of ABO BGS are one or same blood group system.
§ (e.g. Rh-associated glycoprotein gene was not grouped
all located in the paragloboside, which is a particular in Rh blood group system, because Rh antigens are
portion on the red cells of the brain. found in Chromosome #1, while RHAG antigen are
c. Serologic Properties (If a certain antigen of a blood found in Chromosome #6)
group system mounts an IgG or IgM Ab, e.g. Rh • ABO Blood Group System – was the first
discovered Blood Group System by Karl Landsteiner
antigens, all of them are IgG. in 1901.
d. Genetic Control of Antigen Expression (Genes • Usually, ISBT is assigning a 6-digit number of a red
coding for the production of those red cell antigens cell antigen.
are located on the same chromosome.) § E.g. 001001
§ First 3-digits refer to the blood group system where
antigen belongs.
§ Last 3-digits refer to the specific number assigned for
the antigen of a particular blood group system.

M. PETRONIO & ANDREI – TRANSCRIBERS

 Number Blood Group System Red Cell Antigen b. Sex Chromosome: 1 Pair = 2
001001 ABO BGS A Antigen • XX – female
001002 ABO BGS B Antigen
004001 Rh BGS D Antigen
• XY – male
• There are also genes encoded in X chromosome, like
Xg gene and Kx gene.
OTHER TERMINOLOGIES IN GENETICS
Ø Genotype - it is the actual genetic make-up of an individual
Ø Gene - it is the basic unit of inheritance that is located in genes inherited from parents.
chromosomes • Every gene in the body is expressing or encoding a
Ø Chromosome - it is a structure within the nucleus that certain protein that is responsible for a certain trait or
contains DNA. characteristic.
• DNA – contains the instructions on how certain protein Ø Phenotype – it is the physical or observable expression of
will be produced. genes.
CENTRAL DOGMA • Includes Blood type (also called as Blood Group/Red
DNA Replication – mRNA transcription – Protein translation Cell Phenotype)
• When DNA is translated into proteins, that protein will Ø Punnett Square – square used to calculate the frequency
be responsible in giving a particular trait of the resulting genotypes and phenotypes among the
• If you inherited the DNA from your father, who has the offspring of a cross.
A antigen, your father gave you his A gene during the
fertilization process. That A gene in Chromosome #9, ABO BLOOD GROUP/ RED
POSSIBLE GENOTYPE
once it undergone transcription and translation, the CELL PHENOTYPE
product of expression of A gene is the A antigen A1 A1A1, A1O
A2 A2A2, A2O,A1A2
Ø Types of Chromosome
a. Somatic/Autosome: 22 Pairs = 44 (Chromosome 1-44) B BB,BO
• In very somatic chromosome, genes were located A1B A1B
responsible for the encoding or the production of A2B A1B
antigen of a particular blood group system.
• Most of the genes in the blood groups system are O OO
somatic chromosome (Chromosomes #19, #18, #17,
#12, #1, #2) • When doing Red Cell Phenotyping or determination of Blood
Group, you can infer out of a known blood type or blood group,
• There are also chromosomes that contain multiple
on what is the possible blood type of the person.
genes. • If the Blood type of the person is A1, his genotype could either
be A1A1 or A1O.
Chromosome Blood Group System • If his Blood type is B, his genotype can either be BB or BO.
Chromosome #1 Rh gene • Most of the time, the name of the gene and the antigen that it
Duffy gene expressed has the same designation.
Scianna gene § A GENE ------ A ANTIGEN
Cromer gene § B GENE ------ B ANTIGEN
Knops gene • To distinguish, the gene/s must be italicized, and the
antigen/blood type/blood group must be written in
Chromosome #6 Chido/Rodgers gene standard form.
I gene • A1 and A2 are two subgroups of Type A
RHAG gene • A1B and A2B are two subgroups of Type AB
MHC gene • Having said that the name of the gene and the antigen it
Chromosome #7 Kell gene produces, has the same designation.
Yt gene § What gene produces the A1 Antigen = A1 gene
Colton gene § What gene produces the A2 Antigen = A2 gene
Chromosome #9 ABO gene • A gene and B gene – DOMINANT GENE (whatever
Gill gene happens, their products will be expressed)
Chromosome #11 Indian gene • O gene – RECESSIVE GENE (when recessive gene
Raph gene was paired to a dominant gene, dominant gene will
Chromosome #19 Lutheran gene only be expressed)
Lewis gene • Genotype is always in pair (A1A1, A2B) because one
Landsteiner-Weiner gene gene is contributed by the father and the other was
H gene from the mother, which applies to every trait of a
Ok gene person.
§ The genotype in your chromosome #9 where
ABO genes are located, is A1O, will A1 gene
• MHC genes – responsible for the production of HLA
produce its product? Yes, which is A1 antigen.
Antigens which is Chromosome #6.
§ Will there be A1 antigen in your RBC? Yes,
• Is Chromosome #6 only exclusive for MHC genes? No,
expressing Type A blood, particularly, A1
because there are many genes like RHAG gene and I
subgroup.
gene present in Chromosome #6.
§ O gene is recessive gene paired with a
dominant gene A1, will O gene express its
product? No, because only the dominant gene
will be expressed.
M. PETRONIO & ANDREI – TRANSCRIBERS
Using Punnett Square, Chromosome #9 ABO gene
• Father: A1A1 (Type A1) Gill gene
Mother: A1B (Type A1B) Chromosome #11 Indian gene
Child: Raph gene
Chromosome #19 Lutheran gene
A1 A1 Lewis gene
A1 A1A1 A1A1 Landsteiner-Weiner gene
H gene
B A1B A1B Ok gene

a. Probability that child’s genotype is A1A1: 50% Ø DOMINANT GENE – gene whose product is always
b. Probability that child’s phenotype is A1: 50% expressed.
c. Probability that child’s blood type is AB: 50% Ø RECESSIVE GENE – genes whose product will only be
d. Probability that child’s blood type is A1: 50% expressed if inherited in a homozygous way.
e. Probability that child’s blood type is A2: 0% • OO – Type O (only expressed when paired in
homozygous way)
• Father: Type A Ø CODOMINANT GENE – both genes are dominant, so
Mother: Type B product of both genes will be expressed.
Child: Type O • AB gene is a codominant gene, A is dominant, B is
a. Is this possible? Yes, if the father phenotype is AO and dominant. Both genes can express their product.
mother is BO. Ø HOMOZYGOUS GENE – genes comprising a genotype
that are identical. E.g. (AA)
• Father: Type AA Ø HETEROGENOUS GENE – genes comprising a genotype
Mother: Type BB that are different. E.g. (AB, AO)
Child: Type O
a. Is this possible? No. DOSAGE EFFECT

• Father: Type AO
Ø Dosage Effect – stronger agglutinations are produced by
Mother: Type BO
antigens that are expressed by homozygous genes; weaker
Child: (25% Type O; 25% Type AB; 25% Type A; 25%
reactions are produced by antigen expressed by
Type B)
heterozygous genes.
• Happens in,
A O
Blood Group System Mnemonics
B AB BO
MNS My
O AO OO KIDD Kid
• Father: Type AB DUFFY Dug
Mother: Type AO Rh Rhombus
Child: No chance of having type O child. CHIDO/ROGERS Child
(50% Type A; 25% Type B; 25% Type AB)
Genotype Red Cell Antigen Anti-M Antisera
Ø ALLELES – one of two or more genes are occupying the
same locus on the chromosome; other term for genes. MM M antigen 4+
• E.g., AA (an A allele and another A allele)
BO (a B allele and O allele in the same chromosome #9) MN M antigen; N antigen 2+
Ø ANTITHETICAL – a term used to refer to the opposite
allele. • MM gene will produce M antigen
• E.g., BO (B allele antithetical to O allele) • MN gene will produce M antigen and N antigen
• Anti-M antisera will be used to detect if M antigen is
Ø POLYMORPHIC GENE – genetic system that produces present in the red cell.
multiple products. • Because of dosage effect, which among the two
Chromosome Blood Group System antigen is a product of homozygous gene? M
Chromosome #1 Rh gene antigen only.
Duffy gene • Both will be tested positive with Anti-M antisera but MM
Scianna gene gene will give a stronger reaction compare to MN gene.
Cromer gene • MM genotype has more M gene compare to MN gene.
Knops gene
Chromosome #6 Chido/Rodgers gene
I gene Genotype Red Cell Antigen Anti-M Antisera
RHAG gene
AA A antigen 4+
MHC gene
Chromosome #7 Kell gene A antigen; No O
AO 4+
Yt gene antigen
Colton gene

M. PETRONIO & ANDREI – TRANSCRIBERS

 • O gene has no product because it is a silent gene. NULL PHENOTYPES: phenotypes that lack the
• Both will give a stronger effect, since they are both from
ABO Blood Group System. expression of the red cell antigens of a particular blood
• There is no dosage effect in ABO Blood Group System. group systems. (NO ANTIGENS IN THE RED CELLS)
• Whether A antigen came from AO or AA genotype, both will
give the same degree of agglutination or reaction with Anti-A
antisera, since there is no dosage effect in ABO Blood
Group System. May be due to inheritance of:
1. Silent/Amorphic gene: GENES WITH NO
Ø CIS – means that 2 genes are on the same side of the
chromosome. EXPRESSED PRODUCT. Example: O gene (No
Ø TRANS – means that 2 genes are on opposite side of the
chromosome. product; No "O" antigen)
E.g. Rh Genes
• DCE/dce
- Both big D and C are on the same of Chromosome #1 2. Regulator/Suppressor gene: GENES THAT INHIBIT
- Described as “Big D gene is in CIS position with respect
with the Big C gene”.
THE EXPRESSION OF ANOTHER GENE.
• DcE/dCe
- Big D genes and the Big C gene are on the opposite
BLOOD SILENT REGULATOR NULL
sides of Chromosome #1.
- Described as “Big D gene is in TRANS position GROUP GENE GENE PHENOTYPE
compared to Big C gene”
SYSTEM
§ C Trans Phenomenon
– mechanism behind if the Big D and Big C gene are in H hh Bombay phenotype
TRANS position.
– the cause of expression of Weak D or Du Variant RH rr XorXor Rh null

Ø LINKED GENES - there are two genes that are very close to KELL KoKo Kell null
each other.
LUTHERAN LuLu In (Lu) Lu(a-b-)
• In Chromosome #4, M and N genes are very close to one
another, instead of calling that as GENOTYPE, if the genes DUFFY Fy Fy Fy(a-b-)
comprising a genotype are made up of linked gene, it is
called as HAPLOTYPE. KIDD JkJK In (Jk) Jk(a-b-)

Ø HAPLOTYPE – genotype whose genes are linked genes, as a

result the products of linked genes will be both expressed.
• Because they are linked genes, when one is expressed, one NOTES: If you don't have an "H" Antigen your blood type in
will be also expressed automatically. a red cell it would be called as: BOMBAY PHENOTYPE (H
Null Phenotype) - discovered in Bombay, India as a lot of
INHERITANCE PATTERNS residents there has this phenotype

1. Autosomal Dominant: TRAIT WILL ALWAYS APPEAR

WHENEVER THE ALLELE IS PRESENT H gene H antigen - ONLY ANTIGEN in H Blood
2. Autosomal Recessive: TRAIT WILL ONLY APPEAR IF Group System
THE ALLELES ARE INHERITED HOMOZYGOUSLY ‘hh gene NO PRODUCT (No "H" Antigen)
3. Sex-linked Dominant: FATHER TO DAUGHTER
TRANSMISSION OF TRAITS (*Son (Male) will only be a
KIDD BGS:
carrier)
JK GENE NO PRODUCT (*as it is a Silent Gene)
4. Sex-linked Recessive: MOTHER TO SON TRANSMISSION OF
TRAITS (*Daughter (Female) will only be a carrier) JKA GENE JKA ANTIGEN

(Example: Haemophilia A (Who has symptoms? MALES) JKB GENE JKB ANTIGEN
5. Codominant: EQUAL EXPRESSION OF INHERITED ALLELES
*ALL THE GENES OF ALL ABO BLOOD GROUPS SYSTEM JKA JKB JK(A+B+) (blood type)
ARE INHERITED VIA CODOMINANT PATTERN OF
INHERITANCE (EXCEPT XG, KX BLOOD GROUP SYSTEM- VIA JKA JKB JK(A-B-)
SEX LINKED-DOMINANT)
In(Jk) -INHIBITOR
Question: Who will express the Xga antigens on the red cells?
*For a Silent Gene and a Regulator Gene to express a
FEMALE (*Notes: MALE WILL ALWAYS BE A CARRIER ONLY
IN SEX LINKED-DOMINANT) Null Phenotype they must be inherited in a HOMOZYGOUS
PATTERN.
M. PETRONIO & ANDREI – TRANSCRIBERS
 ABO BLOOD GROUP SYSTEM Px's RBC + B serum (Anti-A)= 4+ agglutination - A antigen
Px's RBC + A serum (Anti-B)= 3+ agglutination - B antigen
Ø Most important of all the blood group systems
Px's RBC + O serum (Anti- A,B)= COMPLETE
Ø Transfusion of as small as 0.1ml ABO incompatible
HEMOLYSIS
blood to a recipient can cause IHTR (Immediate
Hemolytic
ABO Blood Group: "AB"
Ø Transfusion Reaction
Ø ISBT No.001 (as it was the first blood group system
2. Backward/ Indirect/ Reverse/Serum Grouping: detection
that has been discovered by Landsteiner in 1901)
of antibodies in the patient’s serum using known red cells.
*Only unique in ABO Blood Group System
Landsteiner Law/Rule: Rule stating that normal, healthy
Sample: Serum
individuals possess ABO antibodies to the ABO blood
Reagents: Known Red Cells
group antigens absent from their red cells.
*Do not use plasma because it forms fibrin clots and
may be mistaken as a positive reaction.
A ANTIGEN in RBC ANTI-B
B ANTIGEN in RBC ANTI-A / Antibody A
2+ to 4+
PATIENT'S
ABO Blood Grouping/Blood Typing:
RED CELL
REACTION
1. Forward/ Direct/ Red Cell Grouping: detection of
WITH:
antigen in the RBC using known antisera.
ABO ANTIGEN/S Known A Known Known Known
Sample: 2-5% Red Cell Suspension (RCS)
BLOOD ON RBC RED cells B cells AB O
Reagents: Antisera (containing ANTIBODIES)
GROUP RED RED
cells cells
3+ to 4+
A Anti-B 0 + + 0
PATIENT'S
B Anti-A + 0 + 0
RED CELL
REACTION
AB No Anti-A 0 0 0 0
WITH: and No

ABO ANTIGEN ANTI-A ANTI-B ANTI-A,B Anti-B

BLOO /S ON (BLUE) (YELLOW (COLORELE O Anti-A, Anti- + + + 0
D RBC BROMTHYM ) SS) B and Anti-
GROU OL BLUE ACRIFLAV A,B
P IN DYE
A A antigen + 0 +
KNOWN O – O CONTROL CELLS (Check the results; For
B B antigen 0 + +
Quality Control)
AB A and B + + +
Ø DETECT PRESENCE OF COLD ANTIBODY
antigen
ANTI-I
O No A and 0 0 0
No B
antigen FORWARD
Px's RBC + anti-A= 4+
B serum: has anti-A Px's RBC + anti-B= 0
A serum: has anti-B Px's RBC + anti-A,B= 4+
O serum: has anti-A,B (Tube Method)
*Slide Method is the least sensitive and least reliable method in
ABO Blood Type: "A"
doing blood typing/ blood grouping/blood phenotyping.
M. PETRONIO & ANDREI – TRANSCRIBERS
REVERSE Populations which can exhibit Group 1 discrepancy:
Px's serum + KA: 0 1. Newborns
Px's serum + KB: 3+ 2. Elderlies
Px's serum +KAB: 3+ 3. Leukemic patients
Px's serum + KO: 0 4. Patients taking immunosuppressive drugs
5. Patient’s with congenital agammaglobulinemia
ABO Blood Type: "A" 6. Patients with BM Transplantation
7. Patients whose ABO antibodies are diluted with plasma
ABO DISCREPANCIES transfusion or exchange
8. ABO subgroups
• Occurs when results of forward grouping does not match with
the result of the reverse grouping or vice versa. 9. Chimerism- presence of two cell populations in a single
• It occurs when unexpected reactions occur in the forward and individual
reverse grouping. (*Check ABO discrepancies! Hanapin mo
kung saan ka nagkulang at nagkamali as a MEDTECH!) RESOLUTION:
• Incubating patient’s serum for 15-30 minutes at 4 degrees
CAUSES: Celsius.
1. TECHNICAL ERRORS • Auto control and O control must always be tested alongside with
• Clerical errors the patient’s sample.
– Mislabeled tubes
– Patient misidentification 3. GROUP 2 DISCREPANCIES
– Inaccurate interpretations recorded • Can cause unexpected reactions in the Forward grouping due
– Transcription error to weakly or missing antigen.
– Computer entry error • Least frequently encountered.

• Reagent or equipment problems Causes:

– Using expired reagents 1. Subgroups of A may be present
– Using an uncalibrated centrifuge 2. Weakened A or B antigen as a result of leukemia
– Contaminated or hemolyzed reagents 3. Hodgkin’s disease
– Incorrect storage temperatures 4. Acquired B phenomenon
5. B(A) phenotype
• Procedural errors 6. Chimerism
– Reagents not added
– Manufacturer’s directions not followed RESOLUTION:
– RBC suspensions incorrect concentration • Same with Group 1
– Cell buttons not resuspended before grading agglutination • Incubating patient’s serum for 15-30 minutes at 4 degrees
Celsius.
2. GROUP 1 DISCREPANCIES • Auto control and O control must always be tested alongside with
• Can cause unexpected reactions in reverse typing due to the patients sample.
weakly reacting or missing antibodies.
• Most common cause of ABO discrepancy.

M. PETRONIO & ANDREI – TRANSCRIBERS

4. GROUP 3 DISCREPANCIES
Frequency Distribution of ABO Phenotypes
• Cause problems in forward and reverse grouping and are due
to plasma proteins abnormalities.
ABO Whites (%) Blacks (%) Asians (%)
which can result to rouleaux formation and pseudoagglutination
Phenotype
- stocking of RBC’s like piles of coins.

Causes:
1. Elevated levels of globulin due to multiple myeloma,
A 40 27 28
Waldenstrom’s macroglobulinemia, plasma cell dyscrasias,
some forms of Hodgkin’s disease.
2. High fibrinogen levels
B 11 20 27
3. Plasma expanders like dextran and polyvinylpyrrolidone
4. Wharton’s jelly( cord blood)
AB 4 4 5
RESOLUTION: O 45 49 40
• Perform saline dilution or saline replacement technique.
• Washing cord cells six-eight times with saline to remove
Wharton’s jelly.
Most common ABO Blood Type: "O"

5. GROUP 4 DISCREPANCIES Second most common ABO Blood Type: "A"

• Due to miscellaneous causes. Third most common ABO Blood Type: "B"
Rarest ABO Blood Type: "AB"

CAUSES:
1. Presence of cold-reactive autoantibodies - ( anti-1)
ABO Compatibility for Whole Blood, RBC and
2. Patient has circulating RBC with more than one blood type Plasma Transfusions
3. Unexpected ABO isoagglutinin
4. Unexpected non-ABO isoagglutinins
5. Cis-AB- refers to inheritance of both AB genes from one RECIPIENT DONOR
parent carried on one chromosome and an O gene
inherited from another parent
ABO Whole Blood Red Blood Plasma
PHENOTYPE Cells
RESOLUTION:
• For cold auto-antibodies- incubate RBCs of patient at 37 A A A, O A, AB

degrees Celsius; treatment with dithiothreitol. B B B, O B, AB

AB AB AB, A, B, O AB

O O O O, A, B, AB

Whole Blood- TYPE SPECIFIC/ EXCLUSIVE (ANG "A" AY

KAY "A" LAMANG!)
Plasma/ Red Blood Cells- TYPE SPECIFIC; HAS AN
ALTERNATIVE

M. PETRONIO & ANDREI – TRANSCRIBERS

 ELUTION: process of dissociating antibody from red cell
(This depends on the type of blood transfusion) surface.
Universal Donor in Red Cell Transfusion: “O”
Universal Recipient in Red Cell Transfusion: “AB” 3. Clinically Significant - capable of causing HEMOLYTIC
Universal Donor in Plasma Transfusion: “AB” TRANSFUSION REACTION (HTR) and HEMOLYTIC DISEASE
Universal Recipient in Plasma Transfusion: “O” OF THE NEWBORN (HDN).

In whole blood transfusion, THERE'S NO UNIVERSAL 4. Produced on 3-6 months after birth - newborn has no RBO

DONOR AND UNIVERSAL RECIPIENT. antibodies yet. (THE BABY NEEDS TO BE EXPOSED MUNA-
PAARAWAN)

ABO ANTIBODIES (anti-A, anti-B, anti-A1, anti-A,B):

*FORWARD TYPING IS THE METHOD THAT COULD ONLY
BE DONE TO BABIES THAT ARE DAYS OLD. (NEWBORNS)
1. Naturally-Occurring/ Non Red Cell Stimulated Antibodies
5. Production peaks 5-10 years of age then decline as we age.
(These are stimulated by related antigen in the environment
such as pollen grains, fungal antigen that resembles the
structure of Human A and Human B antigens (MOLECULAR
MIMICRY) that triggers for the ABO antigens to be produce) REFERENCES
Ø Notes from Sir Joseph Joy Banzon, RMT, MPH
"A" people has anti-B

"B" people has anti-A

2. Predominantly IgM, except anti-A,B (IgG)

ABO can be detected at room temperature; except for anti-A,B

as it is an IgG. Since anti- A,B is an IgG it CAN CROSS THE
PLACENTA.

ANTI-A, AND ANTI-B CANNOT CROSS THE PLACENTA!

*ABO HEMOLYTIC DISEASE OF THE NEWBORN (HDN)

CAN HAPPEN IF:

Mother: Type "O" - has anti-A, B

Child: Type "A", "B", or "AB"

Question: Is HDN common? YES

What blood type has anti-A,B on their serum? "Type O"

NOTE: anti-A,B is inseparable; is not a mixture of anti-A and

anti-B; it cannot be separated even with adsorption with A and
B red cells.

ADSOPRTION: process of removing antibodies in the serum

using known red cells.
M. PETRONIO & ANDREI – TRANSCRIBERS
 INTERNATIONAL SOCIETY OF BLOOD TRANSFUSION (ISBT) BLOOD GROUP SYSTEM
CHROMOSOMAL NO. OF
NUMBER NAME SYMBOL GENE NAME ISBT
LOCATION AGS
001 ABO ABO ABO(ABO) 9q 4

002 MNS MNS MNS (GYPA,GYPB,GYPE) 4q 46

003 P1PK P1PK P1PK (A4GALT) 22q 2

004 Rh RH RH ( RHD,RHCE) 1p 52

005 Lutheran LU LU (LU) 19q 20

006 Kell KEL KEL (KEL) 7q 32

007 Lewis LE LE (FUT3) 19p 6

008 Duffy FY FY (DARC) 1q 5

009 Kidd JK JK (SLC14A1) 18q 3

010 Diego DI DI (SLC4A1) 17q 22

011 Yt YT YT (ACHE) 7q 2

012 Xg XG XG (XG) MIC2 (CD99) X 2

013 Scianna SC SC (ERMAP) 1p 7

014 Dombrock DO DO (ART4) 12p 7

015 Cotton CO CO (AQP1) 7p 4

016 Landsteiner-Weiner LW LW (ICAM4) 19p 3

017 Chido/Rodgers CH/RG CH/RG (C4A, C4B) 6p 9

018 H H H(FUT1) 19q 1

019 Kx XK XK (XK) Xp 1

020 Gerbich GE GE (GYPC) 2q 11

021 Cromer CROM CROM (CD55) 1q 16

022 Knops KN KN (CR1) 1q 9

023 Indian IN IN (CD44) 11p 4

024 Ok OK OK (BSG) 19p 3

025 Raph RAPH RAPH (CD151) 11p 1

026 John Milton Hagen JMH JMH (SEMA7A) 15q 6

027 I I IGNT (GCNT2) 6p 1

028 Globoside GLOB GLOB (B3GALT3) 3q 1

029 Gill GIL GIL (AQP3) 9p 1

Rh-associated
030 RHAG RHAG (RHAG) 6p 2
glycoprotein

nu

M. PETRONIO & ANDREI – TRANSCRIBERS