CHAPTER 8: BLOOD GROUP

TERMINOLOGY AND THE OTHER

BLOOD GROUPS
BLOOD GROUP AND TERMINOLOGY
• A blood group system is one or more antigens produced by alleles at a single gene locus or at loci so closely
linked that crossing over does not occur or is very rare.

• Most blood groups genes are located on the autosomal chromosomes and demonstrate straightforward
Medelian inheritance.

• Most blood group alleles are codominant and express a corresponding antigen. (Example: person who inherits
alleles K and k, expresses both K and k antigen on his or her RBCs.

• Silent, or amorphic, alleles exists that make no antigen, but they are rare. When a paired chromosome carry the
same silent allele, a null phenotype results. (consider a null phenotype when reacts with all test except those
with the phenotype (Lu (a-b-) may be directed against an antigen in the Lutheran system or an antigen
phenotypically related to the Lutheran system. In some blood groups systems, the null phenotype results in
RBC abnormalities.

• Blood group antigens are detected by alloantibodies, which occur naturally (not an immune response). Or can
be a response by the immune system after exposure to on-self RBC antigen introduced by a blood transfusion
or pregnancy.

• Serologic testing determines only the RBC phenotype not the genotype. Genotype involves the actual genes an
individual has inherited
THE LEWIS SYSTEM
• The Lewis blood group system is unique bc the Lewis antigens are not intrinsic to RBCs but are on type
1 glycophingolipids that are passively adsorbed onto the RBC membrane from the plasma.
• The two primary concerns are Le(a) and Le(b). The Lewis gene is located on chromosome 19, as a
secretor gene.
• It was observed that individuals with Le (a+) RBCs were mostly non-secretors of ABH. As a result in
general for adults, Le (a+b-) RBCs are from ABH non-secretors and Le (a-b+) RBCs are from the ABH
secretors.
• Individuals with Le(a-b-) phenotype are neither non-secretors or secretor. This phenotype is more
common in AA population.
• The Le (a+b+) is rare amount AA and whites. More common with Asians.
• Lewis antigens are not expressed on cord blood and often diminished on the mother’s RBCs during
pregnancy. Lewis antigen are found on lymphocytes and plts.
• Lewis antigens are resistant to tx with the enzymes ficin and papain, DDT, and glycine-acid EDTA.
• Please pay close attention to Table 8-6 on page 178.
THE LEWIS BLOOD GROUP

• Phenotype Whites Blacks

• Le(a+b-) 22 23
• Le(a-b+) 72 55
• Le(a-b-) 6 22
• Le (a+b+) rare rare
LEWIS ANTIBODIES
• Lewis antibodies are naturally occurring and made by Le (a-b-) persons. (They occur without any known stimulus).
• They are generally IgM and do not cross the placenta. Lewis antigens are not well developed on fetal RBCs. These antibodies
do not cause hemolytic disease of the fetus and newborn (HDFN). Anti-Le(a) and Anti-Le(b) may occur together. Lewis
antibodies occur quite frequently in the sera of pregnant women who transiently exhibit the Le(a-b-) phenotype.
• Lewis antibodies can bind complement, and when fresh serum is tested, anti-Le(a) many cause in vitro hemolysis of
incompatible RBCs, though this is more often seen in enzyme treated RBCs than with untreated rbcs.
• Anti-Le(a) is the most commonly encountered of the Lewis antibodies and is often detected in room temperature tests, but it
sometimes reacts at 37C and in the indirect antiglobulin test. Rare hemolytic trx reactions (HTR) have been reported with
patient who have anti-Le(a) who were trx with Le(a+) RBCs, so anti-Le(a) that are reactive at 37C, particularly those that cause
in vitro hemolysis, should not be ignored. It then becomes important to make sure that unit that are transfused are compatibly
matched with patient.
• Anti-Le(b) is not as common or generally as strong as ant-Le(a). It is usually an IgM and can bind complement. It is normally
made by Le(a+b-).
• The Lewis antigens are not intrinsic to the rbc membrane and are readily shed from transfused rbcs within a few days of trx.
Also it tends to get neutralized once it enters the recipients peripheral blood stream. For this reason, it is rare to anti-Le(a) or
anti-Le(b) to cause hemolysis of trx cells.
LEWIS BLOOD GROUP SYSTEM
• Phenotypes (Most Common)
AA W

• Le (a+b-) 23% 22%

• Le (a-b+) 55% 72%
• Le (a+b+) Rare Rare
• Le (a-b-) 22% 6%
• Neonates: Type as (a-b-) regardless of which Lewis gene they have inherited
LEWIS RED CELL PHENOTYPES

Genes Lewis Red Cell Phenotype

Le Se Lea- Leb+

Le se Lea+ Leb-

lele Lea- Leb-

le se Lea- Leb- Lec+

le Se Lea- Leb- Lec- Led+

P BLOOD GROUP

• Discovered in 1927 by Landsteiner

• Antigens P1 P p pk Luke
• Luke antigen and disease association
THE P BLOOD GROUP

• The P blood group compromised the P, P1, and P(k) antigens and later Luke (LKE).
• P1 and P(k) are assigned to P1PK group system, as P is assigned to the Globoside blood
group system.
• Exists as glycoproteins and glycolipids
• The P1, P, or P(k) antigens can be found on rbcs, lymphocytes, granulocytes, monocytes.
• The P blood group antigens are resistant to treatment with ficin and papain, DDT,
chloroquine, and glycine-acid EDTA.
• Reactivity of the antibodies can be greatly enhanced by testing with enzyme treated cells.
• Five Phenotypes include P1, P2, P1K, P2K, p
THE P BLOOD GROUP

• Phenotype Antigens Present Possible Antibodies Whites Blacks

• P1 P1, P, (Pk) None 79% 94%
• P2 P, (Pk) Anti-P1 21% 6%
• p None Anti-PP1Pk Rare Rare
• P1k P1, Pk Anti-P Very rare Very rare
• P2k Pk Anti-P, Anti-P1 Very rare Very rare
 THE P BLOOD GROUP SYSTEM
• The P1 antigen is poorly expressed at birth and may tale up to 7 years to be expressed fully.
Antigen strength in adults varies from one person to another. Strength also varies with race.
AA have a stronger expression of P1 than Caucasians.
• The P1 antigen can rapidly deteriorate on storage. When older RBCs are typed or used as
controls for typing reagents or when older RBCs are used to detect Anti-P1 in serum, false
negative reactions may occur.
• Anti-P1: common, naturally occurring antigen, IgM antibody in the sera of O1-individuals.
• Anti-P1 is typically a weak cold reactive saline agglutinin optimally reactive at 4C and not seen
in routine testing.
• Stronger examples react at 37C and bind complement, which is detected in antiglobulin test
when poly specific (anti-IgG and anti-C3) reagents are used. It does not Cause HDN and
rarely associated with HTR.
• Reactions that occur below 37C are considered clinically insignificant.
THE P BLOOD GROUP
• Phenotype (p): Anti-PP1Pk is produced by in early life with out sensitization and reacts
with all RBCs except those of the P phenotype. The Anti-P, anti-P1, and Anti-PP1Pk are
separted through absorption.
• Components of Anti-PP1Pk have been shown to be IgM and IgG. They react over a wide
thermal range and effectively bind complement which make them potent hemolysins.
Anti-PP1Pk has the potential to cause severe HTRs and HDFN.
• This antibody has also been associated with spontaneous abortions in early pregnancy.
Anti-P may occur and has been associated with habitual abortions.
• Anti-P specifically is also associated with cold reactive IgG autoantibody in patient with
Paroxysmal cold hemoglobinuria. This rare autoimmune disorder was common seen in
patient with Tertiary Syphilis. This autoantibody typically does not react in routine test
systems.
THE P BLOOD GROUP

• Other illnesses associated with the P group include

• Paracisitc infections: anti-P1
• Early abortions: Anti-PP1Pk or Anti-P
• PCH- autoanti-P
• E. coli infections (UTI)
• Recent studies have demonstrated that Pk provides some protection against the HIV
infection of peripheral blood mononuclear cells.
THE I BLOOD GROUP SYSTEM
• Both I and i are high prevalence antigens, but are expressed in a reciprocal relationship
that is developmentally related. At birth, infant rbcs are rich in i. I is almost undetectable.
During the first 18 months of life, the amount of i slowly decreases and I begins to
increase until adult proportions are met.
• Some people appear not to change their i status after birth. They become the rare adult i.
• Treatment of ficin and papain enhances reactivity of the I and i antigens with their
respective antibodies
• I substance can be found in saliva and human milk and on lymphocytes and platelets
• During disease, the I antigens may alter
THE I BLOOD GROUP

• Phenotype Anti-I Anti-i Anti-IT

• Adult I Strong Weak Weak
• Cord Weak Strong Strong
• Adult I Weak Strong Weakest
THE I BLOOD GROUP
• Anti-I is a common autoantibody that can be found in virtually all sera, although testing at 4C and or against
enzyme treated RBCs may be required for reactivity. Consistently, strong agglutination with the adult rbcs and
weak or no agglutination with cord or adult i RBCs define its classic activity.
• Autoanti-I is found in the serum of many normal healthy individuals is benign, not associated with in vivo rbc
destruction. Usually weak and naturally occurring saline reactive IgM agglutinin.
• Intubating test in the cold enhances anti-I reactivity and helps confirm the identity. Cold autoabsorption to
remove the autoantibody from the serum may be necessary.
• Pathogenic autoanti-I typically consist of strong IgM aggultinins with higher titers and a broad thermal range of
activity reacting between 30-32. When peripheral circulation cools in response to low ambient temperatures,
these antibodies attach in-vivo and cause autoagglutination and peripheral vascular occlusion (acrocyanosis) or
hemolytic anemia.
• Pathogenic anti-I typically reacts with adult and cord rbcs well at room temp and 4C, and antibody may not be
apparent unless the serum is diluted or warmed to 30-37C.
• Patients with M. pneumoniae often develop strong cold agglutinins with I specifically and can experience a
transient episode of acute abrupt hemolysis just as the infection begins to resolve.
• Anti-i: rare antibody occurs in patients with infectious mononucleosis, cirrhosis, myeloid leukemia, reticulosis
• Anti-I is not associated with HDFN bc antibody is IgM, and the I antigen is poorly expressed on infant RBCs
THE I BLOOD GROUP
• Alloanti-i is a fairly rare antibody that give strong reaction with cord blood rbcs and
adult i rbcs and weaker reaction with adult I RBCs.
• Most examples of autoanti-i are IgM and react best with saline suspend cells at 4C.
• This is not a commonly seen antibody in healthy individuals. Potent examples are
associated with infectious mononucleosis and lymphoproliferative disorders.
• IgG anti-i has also been described and associated with HDFN.
• I and i antigens have been found on wbcs and plts.
MNSS BLOOD GROUP

• Phenotypes
 THE MNS BLOOD GROUP
• M and N antigens are found on a well characterized glycoprotein called
glycoprotein A
• Anti-M naturally occurring saline agglutinin that reacts below 37C. Although we may
think of agglutinating anti-M as IgM, 50-80% are IgG.
• They do not bind complement regardless of IgM or IgG.
• They do not react with enzyme treated cells.
• More common in children than adults and more common in patient with bacterial
infections
• As long as Anti-M does not react at 37C, it is not clinically significant for trx and can
be ignored. When reacting at 37C, compatible cross matched units must be
provided.
• Anti-M rarely causes HTR, decrease red cell survival, or HDFN.
THE MNS BLOOD GROUP: N
• Anti-N: A cold reactive IgM or IgG saline agglutinin that does not bind complement or
react with enzyme treated rbc
• They are weak antibodies and rare antibodies, naturally occurring IgM that react best at
room temperature or below.
• They are not clinically significant unless it reacts at 37C. It has been implicated with rare
cases of mild HDFN.
• Both M and N are easily destroyed by the routine blood bank enzyme ficin, papain,
bromelin, trypsin, pronase, ZZAP, DDT in combination with ficin and papain.
• They demonstrates dosage effect with MNS grouping.
THE MNS BLOOD GROUP: S
• Most examples of anti-S and ant-s are IgG, reactive at 37C and the antiglobulin test.
• They normally develop after RBC stimulation.
• Have been associated with severe HDN and HTR. They have been known to bind
complement
• Units selected must be for trx must be cross match compatible
• Usually reactive at the antiglobulin phase of testing.
• The U antigen is found on RBCs except in about 1% of AA. The RBCs usually type S-s-U,
and these individuals can make anti-U in response to trx or pregnancy. Anti U is typically
IgG and has been reported to cause HTRs and HDFN.
• Anti-U is resistant to treatment with enzymes
MNSS BLOOD GROUP

• Antibodies
• Anti-s and anti-U
• Usually IgG and AHG
• Not destroyed by enzymes
• HTR and HDN
• Anti-U found as warm autoantibody and does not react well with
Rh null cells
• Other antibodies rarely detected but not uncommon (ex. anti-Mg
common antibody)
KELL BLOOD GROUP
• Many antigens in this system and has been given a numerical
nomenclature Six most important

Numeric Alpha Name Incidence

KEL 1 K Kell 10%
KEL 2 k Cellano 99.8%
KEL 3 Kpa Penny 2%
KEL 4 Kpb Rautenberg 99.9
KEL 6 Jsa Sutter Rare (19% Blacks)
KEL 7 Jsb Matthews 99.9%(99.8% Blacks
THE KELL AND KX BLOOD GROUP SYSTEM
• The Kell blood group is only found on RBCs.
• The K antigen can be found on fetal rbcs as early as 10 weeks and is well developed at
birth. The k antigen has been detected at 7 weeks
• K is very immunogenic and appears to be preganacy induced.
• The antigens are not denatured by the routine blood bank enymes ficin and papain but
are destroyed by trypsin and chymotrypsin.
• Please pay close attention to chart on page 192 table 8-15. (K, k, K0, Kx)
• K0 or Knull lack all Kell antigens (K and k)
• Kx: associated with the Kell system and located on the X chromosome
THE KELL AND KX BLOOD GROUP
• Anti-K very common antibody seen in the BB
• Is usually IgG and reactive in the immunoglobin phase
• The antibody is made is response to exposure to through pregnancy and transfusion and can
persist for many years.
• Natural IgM are rare and have been associated with bacterial infections.
• The most reliable method of detection is indirect antiglobulin test. The potentiating medium,
PEG, may increase reactivity.
• Anti-K has been implicated in severe HTRs and HDFN. Still birth has been seen with Anti-K.
When a pregnant women is identified as making anti-K, it is prudent to type the father for the
K antigen. If he is K+, the fetus should be monitored carefully for signs of HDFN.
• Anti-k rare, but can cause HTR and HDFN.
THE KELL AND KX BLOOD GROUP
• Kx is present on all RBCs except those of the rare McLeod Phenotype. K0 and Knull phenotype rbcs have
increased Kx antigen. When Kell antigens are denatured with AET or DDT, the expression of Kx increases.
• K0 RBCs lack expression of all Kell antigens. These rbcs have no membrane abnormality and survive normally in
circulation. The phenotype is very rare.
• Immunized individuals with the K0 phenotype typically make an antibody called anti-Ku that recongnizes the
universal Kell antigen (Ku) present on all rbcs except K0.
• Anti-Ku has been known to cause both HTRs and HDFN.
• McLeod phenotype is very rare. All who have it are very rare, and inheritance is X-linked through a carrier
mother. Phenotype lack Kx antigen. These individuals are known to have a weakened expression of the other
Kell system antigens.
• Mc Leod syndrome
• Reduced expression of Kell antigens
• association with hemolytic anemia and chronic granulomatous disease
• genetics and antigen
THE KELL BLOOD GROUP: MCLEOD
• A significant proportion of rbcs in these individuals with the McLeod phenotype appear
to be acanthocytic with decrease deformability and reduced in vivo survival.
• Have chronic but often well compensated hemolytic anemia (reticulocytosis,
bilirubinemia, splenomegaly, and reduced serum haptoglobin levels).
• These individuals tends to have a variety of muscle and nerve disorders. These individuals
tends to have CPK levels of the MM tpye.
• Chronic granulomatous disease (CGD) are x-linked illness associated with McLeod
phenotype.
THE DUFFY BLOOD GROUP
• Th Duffy antigens that are most important in routine blood banking are Fya and Fyb . They can
be identified on fetal cells as early as 6 weeks gestational age and are well developed at birth.
• Phenotype Whites (%) American Blacks (%) Chinese (%)76
• Fy(a+b-) 17 9 90.8
• Fy(a+b+) 49 1 8.9
• Fy(a-b+) 34 22 0.3
• Fy(a-b-) Very rare 68 0
• These antigens have not been found on plt, wbcs. They have been identified on human tissues.
• These antigens are destroyed by common proteolytic enzymes such as ficin, papain, bromelin,
and chymotrypsin
THE DUFFY BLOOD GROUP
• Anti-Fya is a common antibody and is found as a single specificity or in a mixture of
antibodies. Anti-Fya occurs three times less frequently than anti-K. Anti-Fyb is 20 times
less common than anti-Fya and often occurs in combination with other antibodies.
• The antibodies are usually IgG and react best at the antiglobulin phase. Some examples of
anti-Fya and anti-Fyb bind complement. A few examples are saline agglutinins. Antibody
activity is enhanced in a low ionic strength medium. Because anti-Fya and anti-Fyb do not
react with enzyme treated RBCs, this is a helpful technique when multiple antibodies are
present.
• Anti-Fya and anti-Fyb have been associated with acute and delayed hemolytic transfusion
reactions. Once the antibody is identified, Fy(a) or Fy(b) blood must be given; finding such
units in a random population is not difficult. Anti-Fya and anti-Fyb are associated with
HDN ranging from mild to severe.
THE DUFFY BLOOD GROUP
• Fyx does not produce a distinct antigen but, rather, an inherited weak form of Fyb that
reacts with some but not all examples of anti-Fyb. Fyx has been described in white
populations. Individuals with Fyx may type Fy(b), but their RBCs adsorb and elute anti-
Fyb.
• Anti-Fy3 is a rare antibody made by Fy(ab) individuals who lack the Duffy glycoprotein.
The Fy(ab) phenotype has been found in white, black, and Cree Indian families.1 Blacks
with the Fy(ab) phenotype rarely make anti-Fy3. Examples of anti-Fy3 produced by non-
blacks appear to react with all Duffy positive cells equally well. Those made by blacks are
similar, but they react weakly or not at all with Duffy positive cord RBCs.
THE KIDD BLOOD GROUP
• Antigens for this blood group in Jka an Jkb. They are commonly found on the rbcs.
• 91% of AA and 77% of Caucasians are Jka+; 57% of AA and only 28% of Caucasians are
Jkb-
• Jka and Jkb antigens are well developed on neonates RBCs. Jka can be detected as early
as 11 weeks. Jkb at 7 weeks.
• Although Kidd can be responsible for causing HDFN and HTR, Kidd is not very
immunogenic.
• Kidd is not denatured by papain or ficin. Treatment of RBCs generally enhances reactivity
with Kidd antibodies. They are not affected by chloroquine, DTT, AET, or glycine.
• Kidd is not found on plt or wbcs.
THE KIDD BLOOD GROUP

• Phenotype Whites (%) Blacks (%) Asians (%)

• Jk(a+b-) 28 57 23
• Jk(a+b+) 49 34 50
• Jk(a-b+) 23 9 27
• Jk(a-b-) Exceedingly rare Exceedingly rare 0.9 Polynesians
 THE KIDD BLOOD GROUP
• These antigens are known for demonstrating dosage as well as being in combination with
other antibodies.
• Anti-Jka is more frequently encountered than anti-jkb, but neither antibody is common.
• These antibodies are usually IgG but may also be partly IgM and are made in response to
transfusion or pregnancy.
• Antibody reactivity can be enhanced by using LISS or PEG (to promote IgG attachment)or by
using ficin and papain.
• Many examples of the Kidd antibodies bind complement.
• The titer of anti-Jka or anti-Jka quickly declines in vivo. A strong antibody identified following
a transfusion reaction may be undetectable in a few weeks or months.
• The decline in antibody reactivity and the difficulty in detecting the Kidd antibodies are
reasons why they are common cause of HTRs, especially of the delayed Type.
THE KIDD BLOOD GROUP
• People with the null (a-b-) phenotype lack Jka and Jkb and the common antigen Jk3. This
phenotype is most common in the Polynesian and has been identified in other Asian
populations.
• There are no clinical abnormalities noted with this null phenotype.
• Alloanti-Jk3 is an IgG antiglobulin-reactive antibody that looks like an inseparable anti-Jka Jkb.
Because panel cells are Jk(a) or Jk(b), anti-Jk3 reacts with all RBCs tested except the auto-
control.
• Most blood banks do not have the rare cells needed to confirm anti-Jk3; however, they can
easily determine its most probable specificity by means of antigen typing. The individual
making the antibody will type Jk(ab). Like other Kidd antibodies, anti-Jk3 reacts optimally by an
antiglobulin test, and the reactivity is enhanced with enzyme pretreatment of the RBCs.
• Anti-Jk3 has been associated with severe immediate and delayed hemolytic transfusion
reactions and with mild HDN.
 LUTHERAN BLOOD GROUP

• Two antigens Lua (8%) Lub (99%)

• Other antigens Table 8-12

• Important blood group that demonstrates multiple methods for

inheritance of the null cell type
• Lu a-b- inheritance
• InLu dominate inhibitor gene
• lulu recessive lack of Lu gene
• sex linked inhibitor gene
THE LUTHERAN BLOOD GROUP
• This blood group is seldom seen in the serology.
• Antibodies are seen infrequently
• There is not much clinical significant associated with Lutheran antibodies.
• Although the antigens have been detected on fetal rbcs as early as 10-12 weeks of gestation.
• As a result HDFN is rare and only mild. They have not been detected on plt and wbcs. It has
been found on tissue cells.
• The antigen is resistant to the enzyme ficin and papain and to glycine –acid EDTA trx but are
destroyed by the treatment with the enzymes trypsin and the alpha chymotrypsin.
• Example of anti-Lua are IgM naturally occurring saline agglutinin that react better at room
temperature than at 37C. Few react at 37C by indirect antiglobulin testing . Some are capable
of binding complement , but invitro hemolysis has not been reported.
THE LUTHERAN BLOOD GROUP
• Anti-Lub has been seen in IgM and IgA. Most examples of Anti-Lub are IgG and reactive
at 37C at the antiglobulin phase. The antibody is made in response to pregnancy or trx.

• Alloanti-Lub reacts with all cells tested except the auto control, and reactions are often
weaker with Lu (a+b+) rbcs and cord rbcs. Anti-Lub has been implicated with shortened
survival of transfused cells and post-transfusion jaundice, but severe or acute hemolysis
has not been reported.
• Anti-Lu3 is a rare antibody that reacts with all rbcs except Lu (a-b-) rbcs. It is usually
antiglobulin reactive. The antibody is made only by individuals with the recessive type of
Lu(a-b-)
THE OTHER BLOOD GROUP
OTHER MISCELLANEOUS BLOOD GROUPS
THE DIEGO BLOOD GROUP
• The Diego antigens are well developed at birth and are described as resistant to all standard
enzymes and reducing agents such as dithiothreitol (DTT), papain, ficin, and glycine-acid EDTA.
• Diego system antibodies are sometime IgM, but are usually IgG reactive in the indirect
antiglobulin test.
• Both anti-Dia and anti-Dib are characterized as RBC-stimulated IgG antibodies that have
caused HTRs and HDFN.
• Although both antibodies have been associated with causing moderate-to-severe transfusion
reactions and hemolytic disease of the newborn (HDN), milder forms of HDN are noted with
anti-Dib.
• Anti-Wra has caused severe HTRs.
• Autoanti-Wr(B) is relatively common in the serum of patients with warm autoimmune hemolytic
anemia.
THE YT BLOOD GROUP

• Fairly common antibody to a high prevalence antigen that someone is clinically significant and
sometime insignificant.
• They are variably sensitive to ficin and papain, are sensitive to DTT, and are resistant to
glycine-acid EDTA.
• These antigens develop at birth but are expressed more weakly on cord blood than on adult
rbcs. They are absent from rbcs with PNH.
• These antibodies are IgG and are stimulated by trx or pregnancy
• Yt antibodies have not been known to cause HDFN. Sometimes it can be clinically significant
and others it can be clinically insignificant.
THE XG BLOOD GROUP

• This system only has one antigen: Xga

• 2 phenotypes include Xg (a+) and Xg (a-)
• This antigen is X linked and more common in women. It is destroyed by enzyme
treatments. Approximately 89 percent of the female population expresses Xga , whereas
66 percent of the male population expresses Xga. Thus, the mating of an Xg(a) man with
an Xg(a) woman would produce all Xg(a) daughters and Xg(a) sons.
• The antibodies are usually IgG, which bind complement. They do not cause HTR or
HDFN. They have not been found to be immunogenic.
THE COLTON BLOOD GROUP.
• Three antigens include: Coa, Cob , Coab, Antibodies are rare for Coa and Cob.
• Both anti-Coa and anti-Cob are IgG, RBC-stimulated, and reactive in IAT. Anti-Cob has been
shown to bind complement weakly. Both anti-Coa and anti-Cob have been associated with acute to
delayed transfusion reactions. Unlike the anti-Coa , reports have implicated anti-Cob as causing
subclinical to mild HDN only. Of the known examples of anti-Cob, most were noted in individuals
with multiple antibodies, suggesting that the Cob antigen may be a poor immunogen

• Anti-Co3 is characterized as potent IgG, RBC-stimulated, complement binding, and reacting in

the IAT phase of testing. With regard to clinical importance, the antibody has been associated
with causing severe HDN and one mild hemolytic transfusion reaction (HTR
• So far, only seven cases of the Colton null phenotype have been documented. Disease
associations have linked the Co(ab) phenotype with monosomy-7 of the bone marrow, which
can result in myeloid leukemia and preleukemic dysmyelopoietic syndromes.
THE DOMBROCK BLOOD GROUP
• Doa and Dob are inherited as codominant alleles and are described as resistant to ficin/papain
treatment and sensitive to trypsin, pronase, and reducing agents.
• Four phenotypes have been described in the Dombrock system with the following
frequencies in whites: Do(a+b-) at 18 percent, Do(a+b+) at 49 percent, and Do(a-b+) at 33
percent. The Do null phenotype has been noted infrequently in white and Japanese
populations and, as previously noted, the Gya , Hy, and Joa antigens are also lacking.
• The infrequently encountered Dombrock system antibodies are characterized as weakly
reacting IgG, RBC-stimulated, and unable to bind complement. The Do antibodies react
optimally in IAT with polyethylene glycol or enzyme enhancement.
• Interestingly, all known cases of Gy(a) pregnant woman show the presence of anti-Gya in their
serum, suggesting that the Gya antigen is highly immunogenic. 40 None of the Dombrock
antibodies are associated with clinical HDN, although positive direct antiglobulin testing has
been recorded.
• DO antibodies are reported to cause acute to delayed transfusion reactions.
THE CROMER/ROGERS BLOOD GROUP
• The antigens are located on the C4 complement component and adsorbed from plasma
onto the RBC membrane
• All of the CH/RG antigens are poorly expressed on cord cells, sensitive to treatment
with most enzymes such as ficin/papain and pronase, and resistant to reducing agents
such as DTT
• The nine antigens in the Chido/Rodgers system are located on the complement
fragments C4B and C4A, respectively.
• The clinically insignificant CH and RG antibodies present with weak and nebulous
reactivity at IAT and may be identified by plasma inhibition methods and adsorption with
C4-coated cells
BG BLOOD GROUP
• Antigens include: Bga , Bgb , Bgc
• Related to the human leukocyte antigens, (HLA) on RBCs
• Antibodies are not clinically significant.
• The corresponding Bg antibodies are directed toward human leukocyte antigens (HLA). Bg antigens are gene products of the
major histocompatibility complex (MHC) that are categorized into class I and class II antigens.
• For the purposes of transfusion practice, only class I antigens are addressed here. Class I antigens are assigned into three
groups, HLA-A, HLA-B, and HLA-C, which are distributed on all nucleated cells as well as on a number of nonnucleated cells.
• Bg antigens are resistant to treatment with enzymes (e.g., ficin/papain) and reducing agents such as DTT. Bg Antibodies are
described as “nuisance” antibodies whose reactivity can be destroyed by treating RBC antigens with chloroquine or EDTA
glycine-HCL
• Transient increases in some Bg antigens have been observed in various disease states, such as infectious mononucleosis,
leukemia, polycythemia, and hemolytic anemia.
• The Bg antibodies are characterized as IgG and reacting weakly and variably in IAT.
• The Bg antibodies are widely considered to be clinically benign because they are not associated with causing HDN and, except
in rare instances, HTR. Three cases of HTR have been attributed to Bg antibodies, leading serologists to consider HLA
antibodies as a cause when no RBC antibody is detected
THE GERBICH BLOOD GROUP
• Antibodies are extremely rare:
• Antigens: Ge2, Ge3, Ge4 Low Frequency Antigens: Wb, Lsa, Ana, Dha
• May cause HDN
• Accelerate RBCs destruction
• Naturally occuringl or immune
• Usually have IgG
• IgM forms have been seen
• Non reactive w/ enzyme treated cells.
VEL ANTIGENS

• Antigens: very high frequency

• Antibodies
A. May cause HTR but not HDN
B. Usually IgG
C. Bind Complement
D. IgM in saline agglutinin: that binds complement and may cause in vitro hemolysis
• All information from the PP is taken directly from Modern Blood Banking and Transfusion Practice.
• Though the most important information has been given in PP
• It Is still your responsibility to read the chapter to get a better understand of material.
• I advise that after reading the chapter, you do the review questions in the back of the chapter. This is a
good way to know that you understand the information you has been given to you.
• What you fail to understand, read again and again.You can always mark what is not understood and ask
the questions in class or a personal time.
• This chapter will have questions on your 1st exam this semester.
• After reviewing the BOC, many questions on you State Board will be coming from this area. It is
important that you know the information.