Other blood groups Flashcards
How is the Lewis blood group formed? (Ag)
FUT3 (Le) gene => α-1,4-fucosyltransferase adds L-fucose on GlnNAC on Type 1 precursor => Le Ag
Why is anti-Lea only produced in Le(a-b-) ppl?*
- *Anti-Leb rarely seen
characteristics of Le Aby
- naturally occuring IgM (=can’t cross placenta)
- rarely clinically sig.
- can cause HTR if react at 37ºC or IAT
why is Le Aby rarely clinically sig
- Le Ag poorly developed @ birth
- IgM Ab can’t cross placenta
- Aby can be neutralised w/ Le Ag in plasma
- Le AG dissociate from transfused RBC membrane
characteristics of I blood group (Ag)
- CHO
- IGnT > glycosyltransferase for branching
- Ag: i (linear) ; I (branched)
- i (0-18 months); I (18+)* but some adults not convert i -> I
- precursors to Le & ABO Ag
Characteristics of autoanti-I Aby in I blood group
- reacts optimally at 4ºC
- strongly agglutinates adult RBC (than cord RBC)
- cause problems in pre-t testing & reacts @ RT
Characteristics of Pathogenic autoanti-I Aby in I blood group
- reacts upto 32ºC
- seen in cold agglutaninn syndrome:
• cold @ periphery -> IgM bind to complement
• when goes to torso = warmer -> complement activated = haemolysis
Characteristic of compound anti-I Aby
- require presence of BOTH Ag (I + ABO or Le)
- e.g. Anti-HI:
• react strongly to cells expressing BOTH H & I Ag (= O & A2 cells)
• reacts weakly to cells expressing low levels of H or I Ag (= AB, A, cord RBC)
• naturally occurring IgM Aby
• Optimal react @ ≤RT
• cause HTR (clin. sig) @ 37ºC
common type of D variant in Australia
DVI
CHaracteristics of Cw Ag
- described by Willis (in 1946)
- Low incidence: 1-2%
- Substitution of A -> G in RHCE
Frequency of
• K-k+
• K+k+
• K+k-
- K-k+ = 91%
- K+k+ = 8.8%
- K+k- = 0.2% (hard to find ppl w/ no anti-k)
Describe the Mcleod Phenotype (include more?)
- Lack XK (for optimal Kell Ag expression)
- V. rare X-linked disease
- V. weak Kell Ag expression
- Acantho, aniso, inc retic, inc osmotic fragility, dec haptoglobin
WHy might working with kidd Aby be difficult?
- Dosage
- Weak
- Found in combo w/ other Aby
why doees Anti-Lub Ab react w/ all panel cells except auto
bc High incidence - react w/ all cells
Why is anti-Coa rarely encountered in the lab?
Coa Ag is high incidence
Differentiate the ABO groups and subgroups
Use Ulex europaeus lectin => Binds to H Ag
[H]: O > A2 > B > A2B > A1 > A1B
Rxn: 4+ > 3+ > 2+ > 1+ > Neg > Neg
Characteristics of P Blood group (Ag)
- CHO
- Ag: P, P1, Pk (combo of 2 Ag except P2 phenotype expresses only P)
- glycosyltransferase adds CHO residue on precursor substance
Characteristics of Rh Blood group (Aby)
- Immune
- IgG
- not bind to complement
- react optimally @ 37ºC
- Detect w/ IAT
- Anti -E, -e, -C, -c demonstrate dosage
- Aby can cause HTR & HDNB
Characteristics of Kell Blood group (Ag)
- Protein
- Ag: K & k (& K0*)
- Highly immunogenic
- well developed at birth
- Destroyed by reducing agents
Characteristics of Kell Blood group (Aby)
- IgG
- Detect w/ IAT @ 37ºC
- Anti-K cause HTR & HDNB
- Anti-k hard to find compatible units
Characteristics of Kidd Blood group (Ag)
- Ag: Jka, Jkb & Jk3
- Weakly immunogenic
- well developed at birth
- Enhanced by enzyme
Characteristics of Kidd Blood group (Aby)
Anti-Jka & Anti-Jkb
- IgG
- Delayed HTR, rarely HDNB
ANti-Jk3
- react w/ Jk POS cells
- Causes HTR, mild HDNB