3. Blood groups I Flashcards
ABO common precursor molecule
H
type 1H
soluble antigens present in secretions and plasma
type 2H
antigens present on RBCs
H antigen structure includes an ——– added onto the terminal galactose
L-fucose
O transferase
Fucosyltransferase
A transferase
Acetylgalactosaminyltransferase
B transferase
Galactosyltransferase
A sugar
N-acetylgalactosamine
B sugar
D-galactose
Expression of ABO alleles depends on the —- gene
H
naturally-occurring IgG, reacts with both type A and type B cells
anti-A,B
found in type O people
clinical significance of anti-A,B
able to cross placenta and cause mild HDFN
Tests for ABH secretions may establish true group when…
RBC antigens are poorly developed/absent
+ reaction with subgroup A1 cells
Dolichos biflorus
used to subgroup ABOs based on amount of H present
Ulex europaeus (H lectin)
most H –> least H among subgroups
O → A2 → B → A2B → A1 → A1B
hh
Bombay
antibodies present in plasma of Bombays
anti-A, anti-B, anti-A,B, and anti-H
homozygous hh inherited
classical Bombay
hh, Se
Para-Bombay
Lewis discovery
Mourant in 1946
Le gives fucosyltransferase which adds an L-fucose onto…
N-acetylglucosamine
Le are expressed on ———– adsorbed onto RBCs
glycosphingolipids
newborn Le phenotype
Le(a=b=)
Le + Se phenotype < 6yo
Le(a+b+)
Se gene adds L-fucose onto…
terminal galacose
Le, sese, H
secretions: Lea
RBC: Le(a+b=)
Le, Se, H
secretions: Lea, Leb, H
RBC: Le(a=b+)
lele, sese, H
secretions: none
RBC: Le(a=b=)
lele, Se, H
secretions: H
RBC: Le(a=b=)
Le, sese, hh
secretions: Lea
RBC: Le(a+b=)
Le, Se, hh
secretions: Lea, Leb, H
RBC: Le(a=b+)
lele, sese, hh
secretions: none
RBC: Le(a=b=)
lele, Se, hh
secretions: H
RBC: Le(a=b=)
most common Rh phenotypes in white people
1) R1 or DCe
2) r or dce
3) R2 or DcE
4) R0 or Dce
most common Rh phenotypes in Black people
1) R0 or Dce
2) r or dce
3) R1 or DCe
4) R2 or DcE
Made from pools of human sera
20-24% protein
high protein Rh antisera
Monoclonal IgM suspended in saline
saline Rh antisera
Human IgG with opened S-S bonds, allowing the molecule to span greater distances
chemically modified IgG Rh antisera
Monoclonal IgM blended with polyclonal IgG with a protein concentration = to normal human serum
monoclonal/polyclonal Rh antisera
pros of high protein antisera
rapid; reliable; protein enhances aggregation
cons of high protein antisera
false + with Ab-coated RBCs; must run Rh control; may cause rouleaux; cannot detect weak-D
pros of saline antisera
avoids rouleaux and spontaneous agglutination
cons of saline antisera
less sensitive; not suitable for weak-D
pros of chemically modified antisera
more sensitive; less rouleaux; no control necessary
cons of chemically modified antisera
expensive
pros of monoclonal/polyclonal antisera
IgM works for IS, IgG works for weak-D; little rouleaux; most partial antigens detected
weak-D test procedure
Negative D test at IS…
Incubate at 37° for 15 minutes
Wash and add AHG
A positive indicates weak-D
(Checkcells are used for QC on the AHG if the test is negative)
3 weak-D variations
- position effect (trans to C)
- gene variation (weakened antigens)
- mosaic/partial-D (missing epitopes)
only test for anti-e if donor/patient is…
E+
compound antigen
two genes that produce a unique product when present in the cis-position on a chromosome
c + e in cis position
f compound antigen
allelic variants
genes which vary from the common allele by only a few AAs (missing, additional, or misaligned)
variant form of C seen in 2% of whites
CW
serine residue at position 103 on 2nd extracellular loop of each protein (Exon 2)
G antigen
anti-G is seen with…
anti-C
prenatal patients with anti-G and anti-C can make…
anti-D
how to test for anti-D in somebody with anti-G
remove anti-C/anti-G from plasma by adsorption onto D=, C+, G+ cells, leaving only anti-D in plasma if it’s present
LW is a —— molecule
Intracellular adhesion molecule
differentiate anti-LW from anti-D
Reacts weakly with Rh= cells (anti-D is NR)
Nonreactive with DTT-treated RBCs (anti-D is R)
Nonreactive with pronase-treated RBCs (anti-D is R)
no Rh antigens
Rhnull
Rmod
inheritance of modifier gene XQ, resulting in markedly reduced amounts of antigen
2 ways to inherit Rhnull
Inheritance of 2 amorphic genes at Rh locus
Inheritance of suppressor genes at a regulator locus
abnormalities associated with Rnull (5)
Stomatocytosis
Hemolytic anemia
Increased reticulocytes
Reduced RBC survival
Weakened expression of related antigens (Duffy, S, s, U, LW)
