PRELIM LECTURE L2: ABO BLOOD GROUP Flashcards
who identified the ABO blood group and year
Karl Landsteiner, 1901
SBT # of ABO
SBT #001
only blood group with pre-formed antibodies
ABO
what are naturally occurring antibodies
antibodies that are formed in the serum to antigens that are absent from the RBCs without prior exposure to RBCs through transfusion or pregnancy
transfusion of incompatible ABO type may result:
immediate lysis of donor’s RBCs
most frequent cause of death in FY 2015
transfusion-related acute lung injury (TRALI)
known reagent RBCs used in reverse grouping
A1 and B cells
how is ABO blood group classified
according to antigen present
what substances are chemically similar to A and B antigens
bacteria, pollen particles and other present in nature
T or F:
bacteria can stimulate activation of anti-A and anti-B
T
frequency of blood type from most to least
O>A>B>AB
what is the predominant immunoglobulin in A and B antibodies
IgM
T or F:
ABO antibodies produce strong direct agglutination reactions
T
age where titers are concentrated enough to detect antibodies
3-6 months old
antibodies found in cord blood serum are of what origin
maternal
what antibodies are present in cord blood
IgG maternal antibodies
how to identify the blood type of newborns
forward grouping
at what age does antibody production peak
5-10 years
T or F:
antibody production remains stable with old age
F
antibody production declines later in life
what will happen in wrong ABO group is transfused
rapid intravascular hemolysis
immunoglobulins present in A and B antibodies
IgM, IgG
antibodies present in O
anti-A, anti-B, anti-A,B
anti-A,B reacts with what cells
A and B cells
T or F:
anti-A,B can be separated into pure specificity since it is a combination of anti-A and anti-B
F
anti-A,B is a cross-reacting antibody
what immunoglobulin is anti-A,B
IgG
measuring the amount of IgG anti-A, anti-B, and anti-AB can predict what disease
hemolytic disease of the fetus and newborn (HDFN)
what temperature do immunoglobulins of ABO antibodies react
room temperature (20-24C)
what temperature do immunoglobulins activate complement
37C
what reagent is routinely used for performing ABO confirmation of group O donor units
anti-A,B reagent
what reagent made anti-A and anti-B reagents much more sensitive and can detect weak A and B antigens routinely
monoclonal antisera
reagent anti-A,B can be prepared with the use of what reagents
blended monoclonal anti-A and anti-B; polyclonal human anti-A,B; or blend of monoclonal anti-A, anti-B, and anti-A,B
on which chromosome are the A, B, or O genes located?
chromosome 9
what year was the theory for inheritance of ABO group described
1924
why is the O gene considered as an amorph
because it does not express any antigen (“silent gene”)
the formation of ABH antigen results from the interaction of what three genes
ABO, Hh, and Se
what group of enzyme is produce from Hh gene
glycosyltransferases
what is the basic precursor material from which A,B, and H antigens all originate
paragloboside or glycan
what is the difference between a type 1 and type 2 precursor substance?
Type 1: Beta 1 → 3 linkage between galactose and N-acetylglucosamine.
Type 2: Beta 1 → 4 linkage between galactose and N-acetylglucosamine.
Where are ABH antigens constructed on the type 2 precursor substance?
constructed on the oligosaccharide chains of the type 2 precursor substance on erythrocytes
FUT 1 is for what gene
H gene
FUT 2 is for what gene
Se gene
what is the precursor structure on which A and B antigens are made
H antigen
what chromosome are FUT 1 and FUT 2 genes located
chromosome 19
H gene is for ABO antigens to form where
erythrocytes
Se gene is for ABO antigens to form where
secretions
what age does the expression of A and B antigens on the RBCs fully develop
2-4 years
glycosyltransferase and immunodominant sugar of H gene
a-2-L-fucosyltransferase; L-fucose
glycosyltransferase and immunodominant sugar of A gene
a-3-N-acetylgalactosaminyltransferase; N-acetyl-D-galactosamine
glycosyltransferase and immunodominant sugar of B gene
a-3-D-galactosyltransferase; D-galactose
possible genotype of individuals with H antigen
HH or Hh
sugars occupying the terminal positions of the precursor chain
immunodominant sugars
why does O have the most number of H antigen
amorph=does not produce active transferases=no modification of H substance
phenotype of hh genotype
Bombay phenotype
T or F:
Bombay individuals that inherits ABO genes can have type A, B or O.
F
hh gene= no H substance= no expression of blood groups
why does A group have few amount of H antigen
since A gene elicit high concentration of transferase= increased conversion of H antigen to A antigen sites
number of antigen sites in A1
810,000-1,170,000
number of antigen sites in B
610,000-830,000
number of A antigens on AB
600,000
what is the genotype of secretors
Sese or SeSe
what are secretors
individuals who express ABH antigens in body secretions
T or F:
Se gene affect the formation of ABH antigens on the RBC
F
it affects the formation of ABH antigens on secretions
genotype of non-secretors
sese
types of oligosaccharide chains associated with body secretions
types 1 and 3
types of oligosaccharide chains associated with rbc membrane
types 2 and 4
more abundant oligosaccharide chains
type 1 and 2
fluids in which A, B, and H substances can be detected in secretors
saliva
tears
urine
digestive juices
bile
milk
amniotic fluid
pathological fluids: pleural, peritoneal pericardial, ovarian cyst
who described two different A antigens; year
von Dungern, 1911
what antibodies do A1 react
anti-A and anti-A1
what antibodies do A2 react
anti-A only
weaker serologic reactivity of ABO subgroups is attributed to what
decreased A and B antigen sites on RBC
percent of group A or AB individuals that express A1 or A1B
80%
percent of group A or AB individuals that express A2 or A2B
20%
which A gene produces high concentrations of a-2-N-acetylglycosaminyltransferase
A1
number of antigen sites in A2
240,000-290,000
why does anti-1 not cause transfusion reactions in A1 or A1B cells
since is a naturally occurring IgM cold-reacting antibody; unless it is reactive at 37C
how can A1 and A2 be differentiated
serologically using anti-A lectin
what plant is anti-A lectin made from
Dolichos biflorus
what does anti-a1 lectin agglutinate
A1 or A1B cells
which A subgroup is more reactive with anti-H lectin
A2 (since A2 is glycosyltransferase is less efficient in adding immunodominant sugar to H antigen= more expression of H antigen=more reactive to anti-H)
what plant is anti-H lectin made from
Ulex europaeus
what plant is anti-B lectin made from
Bandeiraea simplicifolia
order of blood groups according to the amount of H antigen from greatest to least
O>A2>B>A2B>A1>A1B
weak subgroups of A
A3, Ax, Aend, Am, Ay, Ael
subgroup of A: mixed field agglutination with anti-A and anti-A,B
A3
subgroup of A:
anti-A: no agglutination
anti-A,B: weak
Ax
subgroup of A:
anti-A and anti-A,B: mixed field
</= 10% rbc agglutinate
Aend
subgroup of A:
anti-A and anti-A: no to weak agglutination
Am
subgroup of A:
no agglutination in both, produce anti-A1
Ay
subgroup of A:
no agglutination in both, do not produce anti-A1
Ael
weak subgroups of B
B3, Bx, Bm,Bel
subgroup of B:
MF agglutination with anti-B and anti-A,B
B3
subgroup of B:
weak to no agglutination with anti-B and anti-A,B
Bx
subgroup of B:
no agglutination with anti-B and anti-A,B
Bm
subgroup of B:
no agglutination with anti-B and anti-A,B; sometimes produces weak anti-B
Bel
who identified Bombay phenotype, year
Bhende, 1952
how many Bombay phenotypes have been reported around the world
130
what happens if no H antigens are formed
no A or B antigens formed
antibodies present in Bombay phenotype
anti-A, anti-B, anti-A,B, and anti-H
Bombay genotype
Oh
Bombay genotype with A/B/AB genes
Oh^A/Oh^B/Oh^AB
why Bombay phenotype cannot receive O blood
because Bombay contains anti-H, O contains H antigens= hemolysis
common sources of technical errors that cause ABO discrepancies
blood sample and test tube labeling error
failure to add reagents
addition of incorrect reagents or sample
cell suspension too heavy or too light
missed observation of hemolysis
uncalibrated centrifuge
overcentrifugation/undercentrifugation
warming during centrifugation
discrepancy type:
weak or missing antibodies
Group I
cause of Group 1 discrepancies
age factor
leukemia
immunosuppressive drugs that cause hypogammaglobulinemia
agammaglobulinemia
bone marrow/HPC transplants
plasma transfusion
resolution for Group I discrepancies
incubate at RT for 15-30 mins or add 1 or 2 drops more plasma/serum or incubate at 4C for 15 mins
discrepancy type:
weak or missing antigen
Group II
cause of Group II discrepancies
subgroups of A or B may be present
Leukemia
Hodgkin
Proteus infection or diseases of digestive tract (leads to acquires B phenomenon)
resolution for Group II discrepancies
incubate RT for up to 30 mins or incubate at 4C for 15-30 mins
discrepancy type:
plasma or protein abnormalities
Group III
cause of Group III discrepancies
rouleux/pseudoagglutination caused by:
plasma expanders, fibrinogen elevation, Wharton’s Jelly, elevated globulins
resolution for Group III discrepancies
wash cells 3x
discrepancy type:
miscellaneous
Group IV
cause of Group IV discrepancies
cold reactive autoantibodies
circulating rbcs of more than one ABO group due to transfusion/marrow transplant
unexpected ABO isoagglutinins
unexpected non-ABO alloantibodies
resolution for Group IV discrepancies
incubate at 37C for short period washed with saline at 37C 3x and retype
if unsuccessful: treat w/ 0.01 M dithiothreitol (DTT)
