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Y4S1 - Haematology > W10TL4 - Other Blood Groups > Flashcards

W10TL4 - Other Blood Groups Flashcards

1
Q

Lewis Blood Group Antigens

A

Two major ag’s - Lea and Leb
CHO in nature
Ag’s are secreted from tissues then adsorbed → RBC
A single L-fucose moiety differentiates the two ag’s
- added by α-1,4-L fucosyltransferase
- encoded by FUT3 (Le) gene
- inheritance is dominant, so only 1 Le allele (Lele) needs to be present for expression
- acts on Type 1 precursor substance only
- added to GlcNAc residue of Type 1 precursor substance
Antigen expressed depends on inheritance of FUT3 and FUT2

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2
Q

Lewis Blood Group Antibodies

A

Naturally occurring, IgM
Anti-Lea is only produced by Le(a-b-) individuals
Anti-Leb is rarely seen
Occur more frequently during pregnancy
Are rarely clinically significant
- Lewis Ag are poorly developed at birth, and IgM antibodies can’t cross the placenta
- neutralised by Lewis Ag’s in plasma
- Lewis Ag dissociate from transfused RBC membrane
Can cause HTR if they react at 37°C or IAT

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3
Q

I System

A

I is the only antigen in the I blood group
A second related antigen, i, is found in the Ii blood collection
Both are produced by glycosyltransferases
- each enzyme is encoded by a different gene
An alloantibody to the i antigen has not been identified

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4
Q

I System Antigens

A 
Two major antigens - i and I
CHO in nature
- i is linear; I is branched
- IGnT encodes the glycosyltransferase responsible for branching
High incidence Ag that vary with age
- 0-18 months = i is expressed on RBCs
- 18+ months = I is expressed on RBCs
- some adults don’t convert from i → I = adult i phenotype
Precursors to the Lewis and ABO antigens
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5
Q

I System Autoanti-I

A

IgM
Found in virtually all sera but is usually benign
Reacts optimally at 4°C
Strongly agglutinates adult RBCs, weakly agglutinates cord RBCs
Can cause problems during pre-transfusion testing if it reacts @ RT
Pathogenic autoanti-I reacts at 32°C and seen in cold agglutination syndrome

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6
Q

Compound Anti-I Antibodies

A

I is found on the same structure as the ABO and Le ag’s
Therefore aby’s against complex ag’s are produced
- require presence of both ag’s for reactivity
Anti-HI is an example
- reacts most strongly with cells expressing both H and I ag’s i.e. O and A2 cells
- reacts weakly with cells expressing low levels of H or I ag

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7
Q

P Blood Group Antigens

A 
CHO in nature
Produced by the addition of CHO residues to a precursor substance by glycosyltransferases
Three major antigens:
- P (028), P1 and Pk (003)
Five (5) RBC Phenotypes
- P1 (P1, P ag's on surface)
- P2 (P ag on surface)
- p (no ag on surface)
- P1k (P1, Pk ag's on surface)
- P2k (P, Pk ag's on surface)
P1 antigen deteriorates during storage → false neg’s
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8
Q

P Blood Group Antibodies

A

Anti-P1
- naturally occurring IgM antibody in P1 neg individuals
- cold reacting, only clinically significant if it reacts @ 37°C
- can cause issues during pre-transfusion testing
Anti-PP1Pk
- naturally occurring IgM and IgG found in p individuals
- mixture of anti-P, anti-P1, and anti-Pk antibodies
- react over wide thermal range, can bind complement
- cause HTR and HDNB, assoc. w/ spontaneous abortion
Anti-P
- naturally occurring in p and Pk individuals
- wide thermal range, can cause HTR and HDNB
- autoantibody is assoc. w/ paroxysmal nocturnal haemoglobinuria

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9
Q

Rh Blood Group

A

C, c, D, E, e
Non-glycosylated proteins
D antigen is highly immunogenic
Enhanced by enzyme treatment
C and c, and E and e, are antithetical (also demonstrate dosage)
Two closely linked loci, RHD and RHCE encode antigens
- RHD encodes D antigen
- RHCE encodes C/c and E/e antigens
Presence of RHD on one or both alleles = D antigen expressed (Rh(D) pos)
Rh(D) neg individuals result from multiple genetic mutations

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10
Q

Causes of Rh(D) Negative Individuals

A
  1. Absence of RHD on both alleles
  2. Presence of the RHD pseudogene (RHDψ)
    - most common cause of Rh(D) neg in Africans (67% of all Rh(D) neg)
    - 37bp duplication of the intron 3-exon 4 boundary introduces a stop codon in exon 6
    - mRNA is not produced from the gene, therefore there is no D protein
  3. Presence of a RHD-CE-D hybrid gene
    - accounts for 15% of Rh(D) neg in Africans
    - the region of the RHCE gene encoding part of exon 3 through to exon 8 is present in the RHD locus
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11
Q

Wiener and Fisher Race Nomenclature

A 
R = D
r = d (absence of D, no d antigen)
C + e = R1 or r'
c + E = R2 or r"
c + e = R0 or r 
C + E + d = ry
C + E + D = Rz
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12
Q

Weak D

A

Expression of the entire/complete antigen is decreased resulting from mutations in RHD
Express complete D antigen so therefore are Rh(D) pos
Multiple mechanisms result in a weak D phenotype:
1. C in trans to D
- also known as the Ceppelini effect
- when C is on the opposite haplotype to D, D antigen expression is decreased
- i.e. Dce/dCe individual express less D antigen on their RBCs than a DCe/dce individual
2. Del
- extremely low expression of D antigen
- reported only in Asian populations
- type Rh(D) neg
- D ag expression identified using adsorption/elution techniques

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13
Q

Partial D

A

Regions of RHD are replaced by regions of RHCE
Protein product is missing part of the D antigen
Partial D individuals are considered either Rh(D) negative OR Rh(D) positive, depending on the whether they are a recipient or donor
Recipient
- partial D individuals express only part of the D antigen
- can produce an anti-D antibody if exposed to the complete D antigen
- partial D recipients should be typed as Rh(D) neg
Donor
- partial D antigen is immunogenic
- it can stimulate the production of anti-D, and can cause HTRs
- partial D donors should be typed as Rh(D) pos

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14
Q

DVI- and DVI+ on Agglutination Cards

A

In Australia, the most common type of anti-D antibodies used is DVI
DVI-
- anti-D won’t agglutinate DVI RBCs
- DVI individuals will be typed as Rh(D) neg
DVI+
- anti-D will agglutinate RBCs
- DVI individuals will be typed as Rh(D) pos

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15
Q

Kell Blood Group

A

K and k
Antithetical, expressed in a co-dominant fashion
Well developed at birth
K is relatively highly immunogenic
Not destroyed by enzymes, but are by reducing agents such as DTT or AET

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16
Q

Kell Blood Group Antibodies

A 
Anti-K
- IgG
- best detected by IAT at 37°C
- causes HTR and HDNB
Anti-k
- very rare
- IgG, detected by IAT at 37°C
- can be difficult to find compatible units for individuals who produce it
17
Q

Other Kell Blood Group Antigens

A

Kpa and Kpb, Jsa and Jsb
Either high incidence (Kpb, Jsb) or low incidence (Kpa, Jsa)
Therefore antibodies are rarely encountered
- most people express Kpb and Jsb, so aby’s aren’t produced
- most people never encounter Kpa or Jsa, so aby’s aren’t common
Aby’s are similar to anti-K in characteristic and clinical significance

18
Q

McLeod Phenotype

A

XK is required for optimal Kell Ag expression
- XK is NOT a Kell Ag itself, but within its own blood group
Individuals lacking XK have McLeod Phenotype
- v. rare, X-linked disease (1:100k)
- v. weak Kell ag expression - acantho, aniso, ↑ retic’s, ↑ osmotic fragility, ↓ haptoglobin
- cardiomyopathy
- neurologic defects
- individuals with chronic granulomatous disease (CGD) can have a similar phenotype

19
Q

Kell Null Phenotype

A

Ko allele = silent
Inheritance of KoKo => RBCs lacking ALL Kell Ag’s
- i.e. K null
- rare (1:25k)
- express XK at ↑ amounts
K null individuals can produce a “universal Kell” aby
- named anti-Ku
- recognises a Kell structure present on all but Ko RBCs
- causes HTR and HDNB

20
Q

Kidd Blood Group

A 
Two major antigens: Jka and Jkb
Jk3 is an ag common to all Jk pos cells
Antithetical, expressed in a co-dominant fashion
Well developed at birth
Poor immunogens
Reactivity is enhanced by enzymes
21
Q

Kidd Blood Group Antibodies

A 
Anti-Jka and anti-Jkb
- usually IgG
- difficult to work with
- demonstrate dosage
- weak
- found in combination with other aby’s
- titre quickly declines in vivo
- not stable on storage
- common cause of delayed HTR, rarely cause HDNB
Anti-Jk3
- reacts to all Jk pos cells
- causes HTR and mild HDNB
22
Q

MNS Blood Group

A

Consists of 5 major antigens

  1. M and N
    - expressed on glycophorin A (GPA; encoded by GPA)
    - destroyed after enzyme treatment of RBCs
  2. S and s
    - expressed on glycophorin B (GPB; encoded by GPB)
    - destroyed after enzyme treatment (except by trypsin)
  3. U
    - universal antigen
    - expressed on GPB
    - not destroyed by enzymes
23
Q

MNS Antibodies

A 
Anti-M and anti-N
- usually naturally occurring aby’s that react below 37°C
- IgM or IgG
- don’t react with enzyme treated cells
- demonstrate dosage
- clinically significant when reactive in IAT @ 37°C
Anti-S and anti-s
- IgG, react @ 37°C, detected by IAT
- demonstrate dosage
- can cause HTR and HDNB
- can be difficult to find compatible units for individual w/ anti-s
Anti-U
- produced in S- s- U- individuals
- immune
- will react to all panel cells, and enzyme treated cells
- can cause HTR and HDNB
24
Q

Duffy Blood Group

A

Consists of five antigens

  • Fya and Fyb (most common)
  • antithetical, expressed in a co-dominant fashion
  • well developed at birth
  • destroyed after enzyme treatment of RBC
  • Fy3, Fy5 and Fy6
25
Q

Duffy Blood Group Antibodies

A 
IgG, detected best by IAT
Anti-Fya more common than anti-Fyb
Demonstrate dosage
Don’t react with enzyme treated cells
Cause acute and delayed HTR and mild to severe HDN
26
Q

Duffy Blood Group Fyx

A

FYX allele
Results in weak expression of Fyb [written Fy(b+w)]
RBCs type Fy(b-) with most antibodies
- Fyb expression is identified via adsorption/elution
Importantly, these individuals cannot produce anti-Fyb aby’s
- therefore can receive Fy(b+) RBCs

27
Q

Lutheran Blood Group

A 
Two major antigens: Lua and Lub
Antithetical, expressed in a co-dominant fashion
Poorly developed at birth
Weakly immunogenic 
Lu(a-b+) has highest frequency
28
Q

Lutheran Antibodies

A

Rarely encountered in the laboratory
Anti-Lua
- naturally occurring, IgM, react best at RT (some will react @ 37°C by IAT)
- mixed field reactivity by tube method
Anti-Lub
- immune, IgG, react best @ 37°C by IAT
- reacts with all panel cells except auto

29
Q

Colton Blood Group

A 
Two major antigens: Coa and Cob
Found on aquaporin-1 - water transporter
Antithetical, expressed in a co-dominant fashion
Cob is a poor immunogen
Co(a+b+) has highest frequency
30
Q

Colton Group Antibodies

A 
IgG, detected using the IAT
Detection is enhanced by using enzyme treated cells
Anti-Coa
- rarely encountered in the laboratory
- can cause HTR and HDNB
- difficult to find compatible cells
Anti-Cob
- can cause HTR and mild HDNB

Y4S1 - Haematology (22 decks)

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