MIDTERM LECTURE L1: THE MNS SYSTEM Flashcards

1
Q

MNS system ISBT

A

002

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2
Q

Landsteiner and Levine found new antigen specificities by immunizing rabbits with

A

human RBCs

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3
Q

Anti-M and anti-N were discovered from the rabbit sera in what year

A

1927

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4
Q

T/F: M and N are antithetical antigens

A

T

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5
Q

Who discovered S antigen

A

Walsh and Montgomery

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6
Q

In what year was S antigen discovered

A

1947

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7
Q

Antithetical partner of S antigen

A

s antigen

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8
Q

s antigen was discovered in what year

A

1951

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9
Q

There is equilibrium/disequilibrium(?) in the expression of S and s with M and N.

A

disequilibrium

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10
Q

In white populations, what is the order of relative frequency for common MNS blood group system haplotypes? (MOST- LEAST frequent)

A

Ns > Ms > MS > NS

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11
Q

In 1953, which scientist named an antibody to the high-prevalence antigen U?

A

Wiener

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12
Q

U stands for

A

for almost UNIVERSAL distribution

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13
Q

The inclusion of U into
the MNS system was due to the observations of which scientist

A

Greenwalt and colleagues

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14
Q

What did Greenwalt and his colleagues observed?

A

All U– RBCs were also S–s–

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15
Q

How many antigens have been included in the MNS system?

A

46 antigens

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16
Q

MNS is almost equal in antigen size and complexity to what blood group system

A

Rh

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17
Q

The genes encoding the MNS antigens are located on what chromosome?

A

chromosome 4

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18
Q

The M and N antigens are found on a well-characterized
glycoprotein called

A

Glycophorin A (GPA)

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19
Q

Major RBC sialic acid–rich glycoprotein (sialoglycoprotein, SGP)

A

Glycophorin A (GPA)

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20
Q

The M and N antigens are antithetical and differ in their amino
acid residues at positions

A

1 and 5

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21
Q

M amino acid at position 1

A

serine

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22
Q

M amino acid at position 5

A

glycine

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23
Q

N amino acid at position 1

A

leucine

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24
Q

N amino acid at position 5

A

glutamic acid

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25
There are about how many copies of GPA per RBC
about 10^6 copies
26
T/F: MNS are not well developed at birth
F (they're well developed at birth)
27
T/F: M and N are located at the outer end of GPA
T
28
M and N are easily destroyed by what routine blood bank enzymes and less common enzymes?
routine blood bank enzymes - ficin - papain - bromelin less common enzymes - trypsin - pronase
29
Can MNS antigens be destroyed by DTT alone?
NO (needs ficin and papain) DTT + f + p = ZZAP
30
Cleaves sialic acid
neuraminidase
31
neuraminidase is also known as
neuraminic acid or NeuNAc
32
M and N antibodies are homogenous/heterogeneous(?)
heterogenous
33
M and N antigens are detected on what tissues
renal endothelium, and epithelium
34
S and s antigens are located on a smaller glycoprotein called
glycophorin B (GPB)
35
S and s are differentiated by the amino acid at what position on GPB?
position 29
36
Amino acid that defines S
methionine
37
Amino acid that defines s
threonine
38
How many copies of GPB per RBC
about 200,000
39
There are about how many times more copies of GPB on S+s– RBCs than on S–s+ RBCs?
1.5 times more copies
40
Are S and s well developed at birth?
Yes
41
T/F: S and s antigens are less easily degraded by enzymes because the antigens are located farther down the glycoprotein
T
42
S and s antigens have enzyme-sensitive sites that are less/more(?) accessible.
less
43
Enzymes that destroy S and s acitivity
- Ficin - papain - bromelin - pronase - chymotrypsin
44
T/F: Trypsin does not destroy the S and s antigens, and neither does DTT, AET, chloroquine, or glycine-acid EDTA treatment.
T
45
Is Anti-M naturally occurring?
yes
46
Anti-M is mostly what class of immunoglobulin?
IgG
47
Anti-M is how many percent of IgG
50-80%
48
Does Anti-M bind complement?
No, regardless of their immunoglobulin class
49
Does anti-M react with enzyme-treated RBCs?
no
50
Anti-M is more common in children/adult(?)
children
51
Anti-M is more common in patients with
bacterial infection and burns
52
Anti-M is pH dependent. What pH?
6.5
53
Anti-M lectin
Iberis amara
54
T/F: As long as anti-M reacts at 37°C, it is clinically significant for transfusion.
F (As long as anti-M doesn't react at 37°C, it is not clinically significant for transfusion and can be ignored)
55
Does anti-M often cause HTRs, decreased cell survival, and HDFN?
no (it RARELY)
56
Anti-N is cold/hot(?) reactive
cold
57
Anti-N immunoglobulin class
IgM and IgM
58
Is anti-N clinically significant?
No, not clinically significant
59
Does Anti-N bind complement?
No, it doesn't
60
Anti-N is seen in which patients
renal patients
61
What substance may alter the M and N antigens?
formaldehyde
62
Anti-N lectin
▪ Vicia graminea, ▪ Bauhinia variegate ▪ Bauhinia purpura
63
Anti-S and anti-s are mostly what immunoglobulin class?
Mostly IgG
64
Anti-S and anti-s are reactive at what temperature
37C
65
Can anti-S and anti-s bind to complement?
yes
66
A few of anti-S and anti-s express optimal reactivity between 10°C and 22°C by what test
saline indirect antiglobulin test
67
If anti-S or anti-s specificity is suspected but the pattern of reactivity is not clear, what can you do that can help in identification?
incubating tests at RT and immediately performing the antiglobulin test (without incubating at 37°C)
68
T/F: Dosage effect can be exhibited by many examples of anti-S and anti-s, but not as dramatic as seen with anti-M and anti-N
T
69
Only how many percent of whites are s–?
11% of whites
70
Only how many percent of blacks are s–?
3% of blacks
71
S– units/s- units(?) are much easier to find
S- units
72
How many percent of whites are S–?
45% of whites
73
How many percent of blacks are S–?
69% of blacks
74
phenotype with partial/complete deletion of GPB
U-phenotype (Universal)
75
U-phenotype (Universal) immunoglobulin class
IgG
76
Can U-phenotype (Universal) cause severe HTR and NDN?
yes
77
RBCs of individuals with U-phenotype type?
S-s-U-
78
phenotype with gene deletion of GPA
En (a-) phenotype (envelope)
79
rare and silent phenotype
Mk phenotype (null)
80
Mk phenotype was named by
Metaxas and Metaxas-Buhler
81
In what year did Metaxas and Metaxas-Buhler find an allele that does not produce M or N
1964
82
RBCs of individuals with Mk phenotype type?
M–N–S–s–U–En(a–)Wr(a–b–)
83
MNS phenotype common in blacks
U-phenotype
84
En (a-) phenotype is resistant to what infection
Pasmodium vivax
85
Who discovered En phenotype
Darnborough and cowrkers and Furuhjelm and colleagues
86
En(a-) phenotype was discovered in what year
1969
87
En(a–) individuals appeared to have RBCs typed as?
M–N– with reduced NeuNAc
88
Most En(a–) individuals produce what antibody
anti-En^a
89
What parasite appears to use alternative receptors, including GPA and GPB for cell invasion?
Plasmodium falciparum