Terry Kotrla, MS, MT(ASCP)BB Unit 9 Other Blood Group Systems Part 2.
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Transcript of Terry Kotrla, MS, MT(ASCP)BB Unit 9 Other Blood Group Systems Part 2.
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Terry Kotrla, MS, MT(ASCP)BB
Unit 9 Other Blood Group SystemsPart 2
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Systems that Produce Cold-Reacting Antibodies
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Covered So FarIiLewisP
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MNSs Blood System (ISBT 002)4 important antigens (more exist):
MNSsU (ALWAYS present when S & s are inherited)
AntibodiesM – antibodies USUALLY reactive at RTN - antibodies USUALLY reactive at RTS – antibodies are clinically significants – antibodies are clinically significantU - antibodies are clinically significant
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MNSs Antibodies – General InformationAll show dosageM & 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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DosageCell IS 37 IgG
1 M+N= (MM) 3+ 1+ 0
2 M+N+ (MN) 2+ 0 0
3 N+N+ (NN) 0 0 0
Cell 1 is homozygous for M, it has a “double” dose of the antigen and all antigens on the cell for this blood group will be M. Notice the 3+ reaction.
Cell 2 is heterozygous, a single dose of each, only 50% of the antigens will be M and 50% will be N. Notice the 2+ reaction
Because there are a decreased number of ANTIGENS you will expect DECREASED serologic reactivity.
When varying strengths of reactions are noted within a single phase of reactivity THINK DOSAGE first and multiple antibodies second.
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Anti-MFrequently detected as a naturally occurring
saline agglutinin at RT testing.Most examples occur WITHOUT red cell stimulus.Weak examples of the antibody can be enhanced
by “acidifying” the serum, lowering the pH to 6.5.RARE examples have been found that are partly
or wholly IgG which have caused HDFN or HTRMOST are clinically INSIGNIFICANT, no HDFN or
HTR.Do NOT need to confirm donors are M negative,
must be crossmatch compatible.Will NOT react with enzyme treated cells.
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Anti-NRarely encountered.IgM Typically weakly reactive at RTConsidered clinically insignificant although
RARE examples of IgG have been observed.Do NOT need to confirm donors are M
negative, must be crossmatch compatible.Will NOT react with enzyme treated cells.
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N Typing ReagentLectin extracted from Vicia graminea has
specificity for N antigen.Add to test RBCs as well as positive and
negative controls.N antigen present = positive agglutination
reaction.N antigen absent = negative agglutination
reaction.
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Variant MN Antigen Mg
VERY RAREPerson with genotype Mg N will test as
M=N+ leading to false conclusion that genotype is NN.
Of primary importance in paternity testing.
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S, s and U AntigensS and s produced by pair of allelic antigens
at locus closely linked to MN locus.
White Black
S+s=U+ 11% 3%
S+s+U+ 44% 28%
S=s+U+ 45% 69%
S=s=U= 0% Less than 1%
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Frequency of MNSs antigens
Phenotypes Blacks (%) Whites (%)
M+ 74 78
N+ 75 72
S+ 30.5 55
s+ 94 89
U+ 99 99.9
High-incidence antigen
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S, s and U AntibodiesClinically significantIgGCauses HDFN and HTRWill NOT react with enzyme treated cells,
antigens are destroyed by enzyme treatment.
Must confirm that donor units are negative for antigen(s).
Donor units must be crossmatch compatible.
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U (Su)The U antigen is ALWAYS present when S and s
are inheritedEstablish as U negative by proving they are S=s=.Can only give U-negative blood units found in <1% of
Black populationSuspect anti-U when a pregnant or previously
transfused black individual reacts with ALL cells tested and has a negative autocontrol.
Will NOT find U negative blood in any population except the black population.
Two potential sources are siblings and rare donor blood.
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Thought…..Can a person have NO MNSs antigens?
Yes, the Mk allele produces no M, N, S, or s antigens
Frequency of 0.00064 or .064%
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Summary of 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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Lutheran Blood Group System (ISBT 005)First example of anti-Lua was found in 1946.Two codominant alleles: Lua and Lub
Antigens are poorly developed at birth.
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Lutheran AntigensGenotype Frequency
Lu(a+b=) 0.15%
Lu (a+b+) 7.5%
Lu (a=b+) 92.35%
Lu (a=b=) Very Rare
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Anti-Lua
Uncommon, usually naturally occurring saline agglutinin.
Not clinically significantReacts at room temperatureRARE Mild HDNNaturally occurring or RARELY immune
stimulated.May agglutinate RBCs in-vitro in MF manner
which is a characteristic helpful in identifying.Donors do NOT need to be antigen typed, must
be crossmatch compatible.
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Anti-Lub
Clinically significant IgG.Has caused MILD HDFN.Has been reported to cause diminished
survival of transfused RBCs (HTR).Rare because Lub is high incidence antigen.Finding compatible blood difficult, 99% of
population is positive.What are two potential sources of
compatible blood?Donors must be antigen negative AND
crossmatch compatible.
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Systems that Produce Warm-Reacting Antibodies
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Kell System (ISBT 006)K antigen first identified in 1946 as causative
antibody in case of HDFN.2 major alleles (over 20 exist)
K (Kell), <9% of populationk (cellano), >90% of population
The K and k genes are codominant alleles on chromosome 7 that code for the antigens
Well developed at birthThe K antigen is very immunogenic (2nd to
the D antigen) in stimulating antibody production
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Kell antibodiesProduced as a result of immune stimulation.IgG (react well at AHG)Clinically significantAnti-K is most common because the K antigen is
extremely immunogenicCaused numerous cases of HTRs both immediate and
delayed.Cause of severe HDFN.
Anti-k occurs much less frequently due to high frequency of antigen, <1 in 500 people are k negative.
Donor units must be antigen negative, crossmatch compatible.
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Other Kell System AntigensOther sets of alleles also exist in the Kell system.Kp antigens
Kpa (Penney, KEL3, 1957) low frequency antigen (only 2%)
Kpb (Rautenberg, KEL4, 1958) high frequency antigen (99.9%)
Js antigensJsa (Sutter, KEL6, 1958), 20% in Blacks, 0.1% in
WhitesJsb (Matthews, KEL7, 1963), is high frequency 80-100%
K is a null phenotype.McLeod
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McLeod SyndromePhenotype has weakened expression of Kell
system antigensAssociated with structural and functional
abnormalities of RBCs and leukocytes. Causes abnormal red cell morphologies and
decreased red cell survival:Acanthocytes – spur cells (defected cell membrane)Reticulocytes – immature red cells
Associated with chronic granulomatous diseaseWBCs engulf microorganisms, but cannot kill (normal
flora)
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Other Kell System AntibodiesSimilar serologic characteristics.Clinically significant, immune antibodies.Frequency of detection influenced by
ImmunogenicityDistribution of antigen in population.
Antibodies are rare which suggests low immunogenicity.
If antigen
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Kidd Blood Group
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
2 antigensJka and Jkb (codominant alleles)Show dosage
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Kidd AntigensWell developed at birthEnhanced by enzymesNot very accessible on the RBC membrane
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Kidd antibodiesAnti-Jka and Anti-Jkb
IgGClinically significantImplicated in HTR and HDNCommon cause of delayed HTRUsually appears with other antibodies when
detected
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Kidd antibodiesAnti-Jk3
Found in some individuals who are Jk(a-b-)Far East and Pacific Islanders (RARE)
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Duffy Blood Group
Phenotypes Blacks Whites
Fy(a+b-) 9 17
Fy(a+b+) 1 49
Fy(a-b+) 22 34
Fy(a-b-) 68 RARE
Predominant genes (codominant alleles):Fya and Fyb code for antigens that are well
developed at birthAntigens are destroyed by enzymesShow dosage
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Duffy antibodiesIgGDo not bind complementClinically significant Stimulated by transfusion or pregnancy but
not a common cause of HDNDo not react with enzyme treated RBCs as
antigens are destroyed/denatured.
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The Duffy and Malaria ConnectionMost African-Americans are Fy(a-b-)Certain malarial parasites (Plasmodium
knowlesi and P. vivax) cannot invade Fya and Fyb negative cells
Antigen acts as a receptor for invasion and are needed for the merozoite to attach to the red cell.
The Fy(a-b-) phenotype is found frequently in West and Central Africans, supporting the theory of selective evolution
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Other Blood Group Antigens…
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Bg AntigensThree (Bennett-Goodspeed) Bg antigens:
Bga
Bgb
Bgc
Related to human leukocyte antigens (HLA) on RBCs
Antibodies are not clinically significant
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Sda AntigensHigh incidence antigens found in tissues
and body fluidsAntibodies are not clinically significantAntibodies characteristically cause mixed
field agglutination with reagent cells
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Xg Blood Group Only one exists (Xga) Inheritance occurs only on the X chromosome
89% Xga in women66% in males (carry only one X)
Men could be genotype Xga or Xg Women could be XgaXga, XgaXg, or XgXg Example: Xg(a+) male with Xg(a-) woman would only
pass Xg(a+) to daughters, but not sons The antigen is not a strong immunogen (not attributed
to transfusion reactions); but antibodies may be of IgG class
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HTLA AntigensHigh Titer Low Avidity (HTLA)Occur with high frequencyAntibodies are VERY weak and are not
clinically significantDo not cause HDN or HTR
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Review
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Cold AntibodiesIgMReact at RT or colderNO HDFN or HTRDonor units do not need to be phenotyped
for antigen.Donor units must be crossmatch
compatible.
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Cold Antibodies (IgM)Anti-Lea
Anti-Leb
Anti-IAnti-P1Anti-MAnti-A, -B, -HAnti-N
LIiPMABHNNaturally Occurring
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Cold Reacting Antibodies
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Warm AntibodiesIgGReact at 37C and, most frequently, at AHGCause of HDFN and HTRDonor units must be phenotyped for
antigen and be antigen negative.Donor units must be crossmatch
compatible.
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Warm antibodies (IgG)
Rh antibodiesKiddKell DuffyS,s
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Warm Reacting Antibodies
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Remember enzyme activity:
Enhanced by enzymes
Destroyed by enzymes
KiddRh
LewisIP
Fya and Fyb M, NS, s
Papain, bromelin, ficin, and trypsin
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Remembering Dosage:Kidds and Duffy the Monkey (Rh) eat lots
of M&Ns
Jka, Jkb, Fya, Fyb, C, c, E, e (no D), M, N, S, s
M&Ns
adapted from Clinical Laboratory Science Review: A Bottom Line Approach (3rd Edition)
M&Ns
Kidd Duffy Rh MNSs
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ReferencesRenee Wilkins, PhD, MLS(ASCP)cm University
of Mississippi Medical CenterAABB Technical Manual, 16th edition, 2008Basic and Applied Concepts of
Immunohematology, 2nd edition, 2008