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SBB > Antigens/Antibodies > Flashcards

Antigens/Antibodies Flashcards

1
Q

What is the linkage for a Type II chain

A

Beta 1-4

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2
Q

What is the linkage for a Type I chain

A

Beta 1-3

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3
Q

Alpha Linkage

A

The hydroxyl group is below the plane

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4
Q

Beta LInkage

A

The hydroxyl group is above the plane

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5
Q

Blood Group vs a collection

A

Blood group has known genetic origin a collection does not

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6
Q

Gene and chromosome for I antigen

A

GCNT2*01 chromosome 6

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7
Q

I blood group ISBT number

A

027

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8
Q

I enzyme

A

Branching Enzyme: B-1,6 acetlyglucosaminyltransferase

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9
Q

Antigens that are destroyed by DTT

A

Lutheran, Dombrock, Cartwright, Indian, Kel

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10
Q

ABO Chromosome

A

9

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11
Q

ABO ISBT

A

001

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12
Q

Blood Group A chemical structure

A

N-acetylgalactosamine

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13
Q

Blood Group B chemical structure

A

Galactose

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14
Q

FUT1

A

Chromosome 19, encode for H, Fucosyltransferase adds fucose group onto Type 2 chains on RBCs

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15
Q

FUT2

A

Chromosome 19, encode for Se, fucosyltransferase adds fucose group onto Type 1 chains in serum/secretions

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16
Q

First autosomal linkage discovered in humans

A

Lutheran and Se on chromosome 19

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17
Q

Lutheran a-b- options

A
  1. autosomal recessive, inheriting two copies of silent gene, true null can make anti-Lua, anti-Lub, anti-Lu3
  2. autosomal dominant inhibitor. In(Lu), inhibitor prevents expression of lutheran through mutations in EKLF (erythroid kruppel like factor) can’t make antibodies (also suppresses P1, Anwj, In, Knops, Cost, Mer2) trace amounts of Lub detected by adsorption/elution
  3. x-linked one family in australia, women are mainly unaffected carriers, unless they receive two copies of mutated x, men are affected. Shouldn’t make Lu3 (also known as LuMod) trace amounts of Lub detected by adsorption/elution
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18
Q

H antigen expression quantity by blood group

A

0> A2>B> A2B> A1> A1B> H deficient

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19
Q

ABO-Histo-Blood group antigens

A

Found in all organ tissues in the body, platelets and environment including bacteria and animals

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20
Q

Anti-B Lectin

A

bandeiraea simplifica

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21
Q

Anti-A1 lectin

A

dolichos bifloris

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22
Q

Anti-H lectin

A

ulex europeas

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23
Q

Anti-A lectins (3)

A

dolichos bifloris, phaseolus limensis, helix pomatia

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24
Q

Acquired B

A

colonic obstruction, colon cancer, sepsis, bacteria carrying deactylases take n-acetyl group off of A antigen, leave only galactosamine, reacts with Anti-B reagent showing both as positive.

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25
Q

Testing to trouble shoot acquired B

A
  1. test against patients own plasma, patients plasma won’t react. 2. add acetylanhydramine, will put acetyl group back onto the galactosamine. 3. using a different monoclonal reagent anti-B to see if the same reaction takes place 4. acidifying the reaction mixture of human RBCs and reagent antibody will stop this result if it’s caused by acquired B.
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26
Q

Lewis antigen frequency (all)

A

Lea-Leb+ (whites 72%) blacks (52%) Lea+Leb+ (very rare, usually in asian populations weak secretor) Lea+Leb- Whites(22%) blacks (19.5%) Lea-Leb- Whites (6%) blacks (28.5%)

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27
Q

FUT3

A

fucosyl transferase, Lewis antigen gene. Adds fucose group on to Type1 chains. Usually weaker to the secretor gene, if there is no secretor fucose then it is Lea if there is already secretor fucse then it is Leb

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28
Q

Who makes Anti-LeAB

A

A, B or AB, Lea- Leb- secretors

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29
Q

FORS1 gene

A

GBGT1

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30
Q

p (null phenotype)

A

Lackin P1, P and Pk. Rare recessive inheritance, missese and nonsense mutation sin the A4GALT gene, Stronger PX2 expression. High Consanguinity (being descended from the same ancestor) rate -Amish Community

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31
Q

All about P1K and P2K Phenotype

A

Both very rare in all populations, recessive traits. Mutations in B3GALNT1- absence of P antigen, all Pk individuals have naturally occurring anti-P in their serum react equally with P1K and P2K

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32
Q

Rare RH phenotypes

A

dcE, DCE, dCE (1% or less) dCe (2%)

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33
Q

Most common White Rh Phenotype and percentage

A

R1 42%

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34
Q

Most common Black Rh phenotype and percentage

A

R0 44%

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35
Q

Most common Asian Rh phenotype and percentage

A

R1 70%

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36
Q

2nd most common White Rh phenotype and percentage

A

r 37%

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37
Q

2nd most common Black Rh phenotype and percentage

A

r 26%

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38
Q

2nd most commone Asian Rh phenotype and percentage

A

R2 21%

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39
Q

Most common white full Rh phenotype

A

R1r

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40
Q

Two most common black full Rh phenotype

A

Ror, RoRo

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41
Q

Difference in RhD and RhCe a.a.,

Difference between E/e and C/c

A

34 to 37 a.a. difference (E)Proline 226 Alanine (e), C (Serine) 103 to Proline (c)

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42
Q

RHD pseudo gene

A

37 b.p. added in exon 4- inactivates. psi in african americans resulting in inactive gene and an early stop codon placement, present in 24% of D negative A.A. Rh negative patient.

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43
Q

3 D negative options

A
  1. Deletion of RHD 2. Pseudogene RHD, Hybrid RHD-CE-D r’s 3. Del
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44
Q

RhAG

A

Rh Glycoprotein, carry ABO structures, Chromosome 6 RhAG gene 409 a.a. Crosses membrane 12 times, absent on RH null U- red cells. RhAG protein is required for expression of Rh proteins

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45
Q

ICAM-4

A

This gene encodes LW (Landsteiner-Weiner) Blood Group Gln-100 (LWa) Arg-100 (LWb)

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46
Q

What percent of Rh negative people exposed to D+ will make antibody

A

50-80% healthy people, 21-22% patients

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47
Q

Ceppellini effect

A

C in trans with RHD, r’ haplotype, Weak expression of D due to being trans to C. Not at risk of making anti-D

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48
Q

Types of Weak D not at risk of making anti-D

A

Types 1, 2, 3 (alterations made in intra-membrane region of the protein structure) not exposed differences

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49
Q

Partial D

A

Lack of or altered exofacial epitopes,

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50
Q

Partial D european

A
  1. DNB 2. DVI 3. DVII most common
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51
Q

Partial D African

A
  1. DIIIa 2. DAR (Weak D type 4.2) most common
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52
Q

DVI

A

Fatal Hydrops Fetalis cases. Anti-D reagents are designed to be negative at IS-Pos at IAT

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53
Q

Partial D Hybrid Alleles

  1. DIIIa
  2. DIVa
  3. DVa
  4. DVI-2,-3,-4
  5. DVII
  6. DFR
  7. DBT
A

Low prevalence Antigen

  1. DAK
  2. Goa
  3. Dw
  4. BARC
  5. Tar
  6. FPTT
  7. Rh32
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54
Q

Del

A

Types as D negative, only absorptions and elutions will detect antigen. Severly reduced protein. Deletion of exon 9 in Asians (10-30%)

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55
Q

Crawford Phenotype

A

Seen in 1/900 blacks. Patient is D negative, there is an amino acid change in RHCE gene makes antigen appear “D-Like: Gamma clone reagent will react with this and make it look like it’s typing D Pos. Patients can make anti-D. ‘ceCF’ phenotype, 3 nucleotide changes 48G>C , 697C>G 733C>G

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56
Q

ceHAR

A

D epitope on RHCE gene. Results from one RHD exon (EXON6?)insterted into the RHCE gene. In serological typing, positive with all anti-D reagents EXCEPT the Ortho Bioclone it’s negative.

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57
Q

P chromosome

A

chromosome 22

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58
Q

Antigen Frequencies, Fors1, NOR, LKE, PX2

A

FORS (0.1%) NOR- 2 families LKE (98%) PX2 (99%)

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59
Q

Left leg branch of the P system

A

Lactosylceramide-> Lactotriaosylceramide->Paragloboside (A4GALT) creates P1 and B3GALNT1 creates PX2

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60
Q

Right leg branch of the P system

A

Lactosylceramide-> (A4GALT) pK-> (B3GALNT1) (GLOB) P globoside (can then be converted to LKE, Nor, FORS1

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61
Q

P1PK system and gene

A

P1 Pk Nor 003 Alpha4Galt

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62
Q

Globoside system and gene

A

P, PX2 028 B3GALNT3

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63
Q

FORS system

A

Fors1

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64
Q

GLOB collection

A

LKE, 209

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65
Q

P1 frequency

A

79% Whites, 94% Blacks

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66
Q

P2 frequency

A

21% Whites 6% Blacks

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67
Q

p, P1K, P2k frequency

A

rare, very rare, very rare

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68
Q

f antigen, antibody

A

ce, anti-f (anti-hrs=anti-f like) c negative and e negative individuals do not have f antigen on red cells, either can be given as acceptable antigen negative in presence of antibody

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69
Q

rhi antigen, antibody

A

Ce, anti-Rhi (anti-hrb=anti-Rhi like)

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70
Q

Rh, Enzymes/DTT?

A

Enhanced by proteolytic enzymes, unaffected by DTT

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71
Q

RH27

A

cE

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72
Q

RH22

A

CE

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73
Q

RH8, RH9

A

Cw and Cx, not a different form a different epitope. Point mutations in the RHCE gene

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74
Q

Cw mutation and what it is

A

122 A>G, antithetical to high prevalence antigen MAR, this antigen is separate from C/c, clinically significant antibody very easy to find antigen negative blood for

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75
Q

Cx mutation

A

106 G>A

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76
Q

MAR

A

High incidence RH blood group antigen, Finnish population. Anti-Mar nonreactive with Rh null, D–. Antithetical to Cw and Cx

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77
Q

G and anti-G

A

G antigen 103Serine position in common between D pos and C pos cells. Most C+ or D+ RBCs are G+. Anti-G appears as an anti-D and an anti-C

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78
Q

Adsorption/Elution anti-G identification

A

First Adsorption r’ (C+G+), second adsorption R0 (D+G+)

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79
Q

Partial e with Anti-e

A

most often found in african americans. This is typically because of variant e genotype, missing a portion of the epitope

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80
Q

Rh null amorph

A

absent Rh protein, reduced RhAG, RhCE altered RHD deleted

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81
Q

Rh null regulator

A

Absent Rh protein, Absent RhAG, RHag mutated/ deleted, Rhnull individuals have no Rh antigens (no Rh or RhAG) on their red blood cells.[44] This rare condition[44] has been called “Golden Blood”.[45] As a consequence of Rh antigen absence, Rhnull red blood cells also lack LW and Fy5 and show weak expression of S, s, and U antigens. Red blood cells lacking Rh/RhAG proteins have structural abnormalities (such as stomatocytosis) and cell membrane defects that can result in hemolytic anemia.[32][44] Only 44 individuals have been reported to have it worldwide.

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82
Q

RH Null, LW presentation

A

All Rh null are LWa-Lwb-

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83
Q

LW cord cell expression

A

Strong regardless of Rh status

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84
Q

Rh negative, LW presentation

A

Lwa and Lwb are weaker on RH negative cells than Rh positive cells

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85
Q

Anti-LW

A

Shows relative anti-D specificity, same reaction with D- and D+ cord cells*** can be a way to differentiate between LW and D antibody. Doesn’t react at all with Rh null cells
For transfusion D-, LW+ units can be transfused. Non-reactive with DTT treated cells

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86
Q

XK gene

A

on X chromosome

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87
Q

K gene

A

on chromosome 7

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88
Q

K antigens

A

K, k, Jsa, Jsb, Kpa, Kpb, normal expression is k, kpb, jsb. any difference comes with mutations

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89
Q

Kpa frequency

A

2% Whites, rare in blacks

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90
Q

Jsa frequency

A

20% in blacks, 0.01 in whites

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91
Q

K frequency

A

9% in whites, 2% in blacks

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92
Q

Ko frequency

A

True Kell null, SNP of Kel*02, no Kell glycoproteins, Cells Kx+s, Ku- Km-

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93
Q

Mcleod Phentype

A

SNP in splice site, protein not formed, no Xk gene, no KX protein no Km, other Kell proteins weak expression, Ku, k, kpb, jsb. Occurs exclusively in males, x-linked. Linked to Chronic Granulomateaus disease

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94
Q

Effect of Gerbich null types on Kell

A

Yus- Kell normal. Gerbich- Kell expression weakened. Leach- Kell expression depressed

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95
Q

k mod

A

SNP at Kel*02, weakened expression of kel glycoproteins, strong kx expression (some make anti-Ku-like antibody that reacts with all but Kmod cells)

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96
Q

K group ISBT #

A

006

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97
Q

Duffy group ISBT#

A

008

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98
Q

Duffy chromosome

A

Chromosome 1

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99
Q

DARC

A

Duffy antigen receptor for chemokines , binds cytokines, especially IL-8, role in inflammation, receptor for malaria, plasmodium vivax, plasmodium knowlesi

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100
Q

Duffy, enzymes

A

Destroyed by enzymes and ZZAP

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101
Q

Expression of Duffy

A

Well developed at birth, reported to weaken when stored, antigens found on RBCs and other tissues, lung, brain, kidney etc.

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102
Q

Fy3 Fy5 frequency

A

100% whites, 32% blacks ( for both)

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103
Q

Fya- Fyb-

A

0% whites (when seen usually true null) 67% black GATA box mutation promoter region. Fy01 or FY02(MORE COMMON) not expressed on rbcs but still expressed on tissues with GATA mutation

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104
Q

Fya+Fyb- frequency

A

91% asian, 10% blacks, 20% whites

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105
Q

Fya+ fyb+

A

48% whites 3% black 9%asian

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106
Q

Fya- Fyb+

A

32% whites 20% black <1% asian

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107
Q

Anti-Fya vs. Anti-Fyb

A

20x more common to see Anti-Fya

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108
Q

Anti-Fy3

A

Found only in Fya-Fyb- (true null) reactivity won’t go away with enzymes, acts like inseparable anti-Fya anti-Fyb

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109
Q

Anti-Fy5

A

Found only in Fya-Fyb- individuals, reacts with all cells except fya-fyb-. Rh null cells regardless of their fya/fyb typing. D– have weakedned Fy5 expression

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110
Q

Anti-Fy6

A

Murine antibody not found in humans

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111
Q

Enzymes Duffy antibodies

A

Fy3 and Fy5 are restistant all other antibodies of Duffy destroyed

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112
Q

Kidd blood group ISBT

A

009

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113
Q

Jk01 and Jk02 chromosome

A

Chromosome 18

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114
Q

Another name of JK

A

HUT 11 Human Urea Transporter 11, uptake of ureaa, prevents RBC shrinkage in hypertonic environment of renal medulla

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115
Q

Jk3 antigen

A

absent/weak in JKa-b- individuals

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116
Q

Jk null

A

True null (homozygous for Jka gene, no jka, jkb or jk3- polynesians or finns) Dominant inhibitor In(Jk) -reported in japanese families no jka no jkb, weak jk3 expression (antigens may be detected by adsorption/elution cannot make antibodies)

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117
Q

Jk antigens on surface

A

Cluster on surface- more likely to activate complement due to close proximity

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118
Q

Jk enzymes, DTT

A

not destroyed by DTT, enhanced by enzymes

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119
Q

Jka+b- frequency

A

26%whites 52%blacks

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120
Q

jka+jkb+

A

50%whites 40% blacks

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121
Q

jka-jkb+

A

24%whites 8%blacks

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122
Q

2M Urea Lysis Test

A

cheap effective way to identify Jka-Jkb- individuals, Cells with normal Kidd antigen will swell and lyse due to HUT11, JKa-Jkb- cells resis lysis by 2M urea but will shrink and shrivel

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123
Q

Can Jk antibodies activate complement

A

yes- clustered on the surface of the red cell

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124
Q

Anti-Jk3

A

looks like inseparable anti-Jka and anti-Jkb. Confirm with adsorption/elution studies, can only be made by true Jk null

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125
Q

MNSs Isbt number

A

002

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126
Q

Glycophorin A translates for

A

M and N and Ena

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127
Q

Glycophorin B translates for

A

S and s and U

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128
Q

Mur+

A

From GYPA antigen more common in SE asia, normally low prevalence but up to 90% in Taiwan. Hybrid M/N antigen, significant antibodies can form

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129
Q

What Differentiates s from S

A

snp at AA 48 defferentiates S(Met48) from s(48Thr)

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130
Q

Is there more GPA or GPB on RBCS

A

GPA. 10^6 copies per cell compared to around 200,000 GPB

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131
Q

What aids in negative charge of red cells

A

MNS glycophorins rich in sialic acid with negative charge

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132
Q

Difference in M and N

A

M a.a.1-Serine a.a.5-Glycine. N aa1-Leucine a.a.5-Glutamic acid

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133
Q

MNS- enzymes

A

M, N S, s destroyed by enzymes, U is resistant Ena is variable. EnaTS- Typsin sensitive, EnaFS-ficin sensitive, EnaFR- Ficin Resistant

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134
Q

Lacking GPA

A

M-N- Ena- Wra- Wrb-. GPA closely associated with Band3 and Diego system. GPA is required for expression of wright b.

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135
Q

Mg

A

in GPA lacking individuals- low resulting from gene rearrangement

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136
Q

Lacking GPB

A

S-s- U variable Dantu+

137
Q

MkMk

A

Lacking both GPA and GPB, M-N-S-s- Ena- Wra- Wrb- U-

138
Q

Anti-N lectin

A

Vivia graminea

139
Q

Anti-M and acidified serum

A

enhanced reactivity

140
Q

Anti-N

A

Associated with Dialysis equipment sterylized with formaldehyde- Anti-NF

141
Q

Band 3 Gene

A

SLC4A1 solute carrier family 4 member 1, chromosome 17

142
Q

Band 3 also known as

A

Anion Exchanger 1 AE1, interacts with membrane skeleton proteins, including ankyrin

143
Q

Diego Gene

A

DI

144
Q

of antigens in Diego system

A

22

145
Q

High incidence Diego antigens

A

Dib Wrb DISK

146
Q

Low incidence Diego Antigens

A

Dia Wra WU and 16 others

147
Q

First autosomal linkage discovered in humans

A

Lutheran to secretor gene on chromosome 19

148
Q

Lutheran anitgens #

A

24 antigens, most are high prevalence, not LUa

149
Q

AUa and AUb

A

Auberger, part of the lutheran blood group Aua (80% whites) Aub (51% whites, 98% blacks)

150
Q

In(Lu) also represses the expression of:

A

P1 AnWj, In, KNops, Cost, and Mer2, CD44

151
Q

Lutheran Antibodies

A

Fragile, loose, Mixed field agglutionation. No HDFN, Placenta is coated in Lutheran glycoproteins. Lu3 reacts like an indecipherable Lua,Lub antibody, made by true Lutheran null

152
Q

Lutheran enzymes/DTT

A

resitsant to enzymes destroyed by DTT

153
Q

Cartwright gene

A

Acetylcholinesterase AChE

154
Q

GPI-liked antigens

A

Cartwright, Dombrock, Cromer, JMH and EMM

155
Q

Cartwright Null

A

No true null known, PNHIII RBCs can type Yta- Ytb- transiently

156
Q

Cartwright Prevalence

A

Yta- high in all populations Ytb- 8% whites and blacks 26% israeli descent

157
Q

Cartwright Enzymes/DTT

A

destroyed by enzymes and DTT

158
Q

Xg blood group

A

XG gene-first blood group assigned to X chromosme . Escapes X-inactivation (Lyonization) , X linked dominant inheritance

159
Q

Prevalence of Xg

A

89% females 66% males. CD99- High prevalence

160
Q

XG enzymes/DTT

A

susceptible to enzymes (FICIN), resistant to DTT

161
Q

Colton Blood Group System Antigens

A

4: COa COb CO3 and CO4 all but COB are high prevalence (COB=10%)

162
Q

Coa-Cob-

A

can make anti-Co3

163
Q

Colton antibodies

A

Implicated in severe HTR AND HDFN

164
Q

Colton gene

A

Aquaphorin 1 AQP-1

165
Q

Gerbich Phenotype

A

-G2 -G3 G4 Lacks GPD altered GPC

166
Q

Yus Phenotype

A

-G2 G3 G4, Weakened Vel and Kell, Lacks GPD altered GPC

167
Q

Leach Phenotype

A

-G2 -G3 -G4, weakened Vel and Kell; hereditary elliptocytosis. Lacks both GPC and GPD

168
Q

Gerbich antigens

A

12 antigens 5 low prevalence 7 high prevalence

169
Q

GPC and GPD

A

interacts with protein 4.1 and p55 maintains membrane stability

170
Q

Protein 4.1 defiiciency

A

RBC abnormalities and weakened Gerbich antigens

171
Q

GPC Receptor

A

for plasmodium falciparum and Influenza A/B

172
Q

Gerbich Prevalence

A

99% of population has G2 G3 G4. up to 50% Melanesians are GE: -2, -3, 4 and have greater resistance to malaria

173
Q

Gerbich enzymes

A

Fly like a G3- Resistant to enzymes. G2 and G4 are susceptible to enzymes

174
Q

Gerbich antibodies

A

G2 and G3 have been implicated in AIHA and HDFN and may bind complement. Can be naturally occuring or immune stimulated

175
Q

Cromer blood Group system located on:

A

DAF- Decay accelerating Factor or CD55. GPI linked

176
Q

Cromer antigen #

A

18 antigens (Viktor Crum’s age), most are high prevalence including Tca and Wesb. Only 3 low: Tcb TcC, Wesa

177
Q

Cromer enzymes

A

Weakened by DTT, resistant to enzymes

178
Q

Inab phenotype

A

Cromer null, can make anti-IFC , no excess hemolysis due to DAF deficiency due to CD59 similar role

179
Q

DAF

A

“cd55” prevents conversIon in complement cascade, similar function to CD59

180
Q

Dombrock disease association

A

loss of Dombrock associated with PNH III

181
Q

Dombrock cell association

A

GPI-LIINKED

182
Q

Gya-

A

null phenoype absence of dombrock glycoprotien

183
Q

Dombrock antigens and prevalence

A

Doa (67) Dob(82) Gya(100) Hy (100)Joa (100-very rare in blacks)

184
Q

Dombrock enzymes/Dtt

A

DTT sensitive, enhanced by enzymes

185
Q

Dombrock antibodies

A

have been implicated in acute and delayed HTRS No HDFN, though DAT may be positive

186
Q

Indian Blood Group System antigens/location

A

CD44 Ina-low Inb-high

187
Q

Indian blood group enzymes and DTT

A

destroyed by enzymes and DTT

188
Q

Indian associated with Lutheran

A

In(Lu) individuals have weakened expression of Indian antigens

189
Q

Indian antibodies

A

No HDFN reported- DAT may be positive, anti-Inb has been reported to cause HTR

190
Q

Vel Blood Group system

A

High prevalence antigen, Vel- is rare in all populations, more common in norwegians and swedes

191
Q

Vel enzymes/DTT

A

enhanced by enzymes variable with DTT

192
Q

Anti-Vel

A

caused severe HTR rare HDFN, can fix complement mostly IgM not naturally occuring reactive at 37 and IAT

193
Q

Scianna blood group ISBT

A

013

194
Q

Scianna number of antigens

A

7, 2 low prevalence Sc2 Rd

195
Q

Scianna chromosome

A

1

196
Q

Scianna enzymes and DTT

A

resistant

197
Q

Fya and Fyb frequency in whites

A

Fya (68%) Fyb (80%)

198
Q

Carbohydrate blood groups

A

ABO, H, I P1 and P, Lewis

199
Q

i adult

A

More common in asians could present with or without cataracts, HEMPAS

200
Q

P antigen is receptor for

A

Parvovirus B19 and E. Coli

201
Q

P1 antibody neutralization

A

hydatid cyst fluid and pigeon egg whites

202
Q

Amino acid sequence for the M antigen

A

ser-ser-thr-thr-gly

203
Q

Mta antigen

A

MN blood group- results from a SNP on the GYPA theronine to isoleucine position 58

204
Q

Vr antigen

A

GYPA SNP Ser47Tyr change

205
Q

MNSs antigens associated with recombination evens

A

Stone A (Sta) Dantu, Henshaw (He) Miltenberger (Mia)

206
Q

Ena-

A

less than 1% lack of GYPA due to multiple different mutations, has some resistance to plasmodium falciparum due to GYPA being a receptor

207
Q

Gp.Nob

A

GYPA SNPs position 68 arganine-threonine and 71 tyrsoine-serine

208
Q

‘N’

A

N like antigen- same 5 terminal amino acids in GYB as in GYA that produce N, appears as an N like antigen (‘N’) even people lacking N won’t make anti-N when exposed, Anti-N is almost exclusively made in african americans lacking the GYB (U-s-S-)

209
Q

Anti-P,P1Pk

A

very rare, acute HTR and early spontaneous abortions

210
Q

Whites Rh phenotype prevalence in order

A

R1>r>R2>R0

211
Q

Blacks Rh phenotype prevalence in order

A

R0>r>R1>R2

212
Q

D negative phenotype by race

A

Whites: Deletion of RHD gene (inheritance of two copies of deleted D) Blacks: point mutation in RHD gene “pseudogene” Asians: Have inactivated Rh gene.

213
Q

Weak D type common in caucasians

A

Type 1

214
Q

Most common partial in whites

A

DVI (D6) - monoclonal reagents usually type these as D negative, therefore patient isn’t typically exposed

215
Q

Knops antigen also known as

A

CR1 -complement receptor one

216
Q

P antibodies that cause spontaneous abortions

A

anti-P, anti-PP1PK (formally Tja-)

217
Q

LE3

A

also known as Lex, Leab, CD15- found in A,B,AB Lea-b- secretors

218
Q

r’s

A

look this up!! —RHD-CE-D s hybrid gene characteristic of the(C)ce s haplotype that produces c, VS, and abnormal C and e, but no D.

219
Q

chromosome of RHAG

A

chromosome 6, absent on RHnull, U- red cells

220
Q

Weak D type 1 specific mutation

A

Val270Gly

221
Q

Weak D type 2 specific mutation

A

Gly385Ala

222
Q

Weak D type 3 specific mutation

A

Ser3Cys

223
Q

Anti-RH29

A

present in Rh null individuals “total Rh” is another name for this antigen

224
Q

Lutheran antigens

A

24 antigens, low prevalence Lu9 and Lu14 high prevalence Lu6 and Lu14 (antithetical to Lu9 and Lu14) Aua (90%) Aub (51% caucasions 98% blacks)

225
Q

Band3 antigens

A

22 antigens in system: Diego, DISK, Wright, Wu and more, mutations can result in abnormal RBC membrane-ovalocytes/spherocytes

226
Q

S a.a. vs. s a.a.

A

S (Met48) s(Thr48) one of the first SNPs discovered!!

227
Q

Last five amino acids of GYPB

A

Leucine -Serine -Threonine -Threonine -Glutamic acid

228
Q

Last five amino acids of GYPA

A

serine -serine-threonine -threonine- glycene

229
Q

Pevalence of Lutheran antigens

A

92.4% Lua- Lub+ ~7% heterozygous 0.2% Lua+Lub-

230
Q

Anti-Wra

A

often naturally occurring

231
Q

High prevalence Diego antigens

A

Dib+ and Wrb+ and DISK

232
Q

Anti-Wrb behavior

A

IgM and IgG, DAT positive but no clinical HDFN present

233
Q

Wr is not expression in individuals deficient in what?

A

GYPA

234
Q

Weak D type one SNP

A

valine to glycine 270- most common weak D type

235
Q

New antigen formation in some Partial D’s example:

A

DVI red cells have BARC antigen.

236
Q

BARC antigen

A

new antigen formation in DVI partial type- due to gene recombination and formation of new antigen

237
Q

DAK antigen

A

new antigen formation in DIII individuals

238
Q

Tar antigen

A

new antigen formation in DVII individuals

239
Q

FPTT

A

new antigen formation in DFR individuals

240
Q

Rh32

A

new antigen formation in DBT individuals

241
Q

Goa antigen

A

new antigen formation in DIV individuals

242
Q

Dw

A

new antigen formation in DV individuals

243
Q

KLF1

A

on chromosome 19- kruppel like factor- a transcriptional factor essential for terminal differentiation of red cells- heterozygosity for nucleotide changes in KLF1 is responsible for dominant Lua-Lub- phenotype of In(Lu)

244
Q

Lu mod

A

expression decreased of Lutheran antigens (in In(Lu) decreased expressions of P1, Inb and ANWJ antigens as well) Lu mod is the name for X linked Lutheran null

245
Q

GATA-1

A

encoded by GATA-1 gene essential for erythroid and megakaryocyte differentitation. changes lead to X-linked type of Lumod (Lua-Lub-)

246
Q

KPA+ effect on Kel antigens

A

Kpa+ cells adversly affect the trafficking of the KEL glycoprotein to the surface of the red cell. Kel expression is weakened (greatly reduced amount of anitgen on surface of the red cell)

247
Q

RHAG chromosome

A

chromosome 6

248
Q

Wrb connection to GYPA

A

requires amino acids (75-99) of GPA to be present on the red cells membrande in order for Wrb to be expressed.

249
Q

Rh null cells- other groups affected

A

LW antigens lacking. and lack or reduced expression of U and S/s antigens. lacks Fy5

250
Q

carbohydrate antigen chain type

A

oligosaccharide chain assembled by step-wise addition of monosaccharides

251
Q

frequency

A

% of the population- in genotypic terms

252
Q

prevalence

A

denotes phenotypic terms - how many people have the trait (not genetic carriers of disease)

253
Q

chimerism

A

dual populations of cells. artificially induced chimerism- A person transfused with O blood- both populations of cells present=mixed field. True chimerism very rare- dual population of cells derived from more than one zygote.

254
Q

Twin chimera (2 different types)

A

can absorb demised twins cells in utero and create two different cell populations. (blood vs. tissues different cell populations) this would be of course a fraternal twin, Identical twins would be…identical therefore no difference would be shown. can also occur without fetal demise through channels linking the two twins blood lines, can at some point become mixed and seen as self-not foreign so antibodies against are never aquired.

255
Q

tetragametic chimeras

A

(dispermic) two different sets of DNA, two eggs fertilized by two sperm, join together

256
Q

BMT chimerism

A

two different cell populations are showing, one from the patients original blood line and the second from the transplanted. the blood should be from the donor’s cells transplanted however the tissues in the persons body will be the original cell line.

257
Q

S nucleotide change to s

A

T143C (T being S and c being s)

258
Q

Genetic testing for presence of Dombrock antigens

A

Dombrock antigens Doa and Dob notoriously difficult to test for due to lack of anti-sera, need to use validated patient antibody sample, difficult to find, therefore genetic testing is a good substitution.

259
Q

Specificities of antibodies(antigens) unavailable for mass donor screening

A

Hy, Joa, Jsa, Jsb Cw V VS

260
Q

Rh typing in donors- genotyping improvement

A

Del and certain Weak D’s or partial D’s in donors are not caught as D positive and are labeled D negative at donor centers due to lack of positive result when performing weak D testing. These units are labeled as D negative and have been shown to cause alloimmunization in D negative individuals. Molecular testing would improve this process by allowing the labeling of D positive for these unique blood types.

261
Q

DNA testing in blood bank

A

typically targets a single SNP or a few SNPs associated with a particular antigen expression. Cannot sample every nucleotide in the gene. Cannot detect and inhibor that causes silent gene expression In(Lu) only detect the lutheran genotype of person.

262
Q

GATA box mutation

A

-67T>C change in promoter region of Duffy gene. prevents transcription of Fya and Fyb on red cells but not on all tissues within the body. ( typically seen in homozygosity of Fyb with gata box mutation), included in african american genotyping.

263
Q

Testing for GYPB*S

A

must aslo test for C>T change at 230 in GYP*B exon 5, or a change in intron 5 (+5g>t) both changes prevent expression of S antigen in african americans.

264
Q

Fyx

A

presence of altered Fyb allele that encodes an amino acid chance, causing greatly reduced expression of Fyb antigen. Type Fyb- with most serologic reagents. European ancestry 2%

265
Q

Kidd expression different ethnicity

A

Silincing mutations associated with loss of Kidd antigen occur in asians. nucleotide chances encoding amino acid changes taht weaken kidd expression occurs in a.a.’s

266
Q

Carbohydrate (histo blood groups)

A

ABO, H, I, P1PK, GLOB, Lewis, FORS

267
Q

Frequency of f(ce)

A

W-65% B-92%

268
Q

Frequency of Ce (Rhi)

A

W-68% B-27%

269
Q

Frequency of Cw

A

2% whites

270
Q

Frequency of V

A

30% Blacks

271
Q

Frequency of Vs

A

32% blacks

272
Q

Frequency of hrs

A

98% blacks

273
Q

Frequency of Goa

A

low

274
Q

Frequency of Rohar (DHAR)

A

<1% Germans

275
Q

Frequency of MAR

A

high frequency

276
Q

freguency of crawford phenotype

A

<1% blacks

277
Q

Another name for Band 3

A

Anion Exchanger 1 (exchanges Cl- and HCo3)

278
Q

Gene Diego/Band3

A

Chromosome 17 SLC4A1

279
Q

Which antibodies of the Diego system have severe HTR and HDFN

A

Dia, Dib, Wra (not Wrb)

280
Q

Gene Colton antigen

A

AqP1

281
Q

Gerbich antigens populatin correllation

A

50% melanesians are G-2,-3, 4 and resistant to malaria

282
Q

Gerbich affect on other antigens

A

G-2,-3,4 and G-2,-3,-4 have weakened Kel and Vel expression

283
Q

Leech phenotype disease association

A

Lacking GPC and GPD- hereditary eliptocytosis

284
Q

Which Gerbich enzymes are/is resistant to enzymes

A

G3 (G2 and G4 are destroyed by enzymes)

285
Q

condition that weakens Gerbich antigens

A

Protein 4.1 deficiency, causes RBC abnormalities as well

286
Q

Cromer belongs to what family

A

the complement activation family

287
Q

Cromer- how many antigens are low prevalence antigens

A

3: Tcb, Tcc, Wes a

288
Q

which bllod group antigens are carbohydrates

A

ABO, Lewis, P1Pk, Globoside, I and FORS

289
Q

where do the glyocosyltransferases remain to act

A

in the golgi, add on specific sugars to growingoligosaccharide chain before it goes to surface.

290
Q

What is the immunizing source of ABO antigens

A

gut and environmental bacteria, possess abo-like structures.

291
Q

Pr antigens

A

Pr1 and Pr2, present on cord cells and adult cells in the same concentration. ‘Native MN glycoproteins’ N-acetylneuraminic acid, destroyed by enzymes. Treatment of neuraminidase decreases antigenicity.

292
Q

Gya, Hy, and Joa

A

Gregory, Holly and Joseph all dombrock antigens.

293
Q

Dombrock

A

‘dumb jock’ GPI linked protein, hangs on with brute strength, not into art (ART4 gene)

294
Q

H antigen- sugar pattern

A

Galactose-n-acetyl-galactosamine- galactose-fucose.

295
Q

anti-ALG and Lutheran

A

anti-lymphocyte globulin, given to patients in transplant rejection specifically renal transplant. anti-T cell antibodies. Causes cross reactivity with Lutheran, normally pan reactive, but when diluted has a lutheran specificity that makes it appear like an anti-Lutheran (would have to give null blood normally, but consider that it could be ALG instead.)

296
Q

P1PK blood group antigens

A

P1, Pk, NOR

297
Q

GLOB blood group antigens

A

P and PX2

298
Q

Globoside collection antigens

A

LKE (FORS has it’s own blood group system 031)

299
Q

pk phenotype lacks….

A

P, PX2, LKE

300
Q

Where is P1 expressed, where is P and Pk expressed

A

P1 expressed only on red cells, P and Pk expressed on many different tissues, P expression on red cells very rich

301
Q

LKE

A

(Luke antigen) an elongation from the P antigen

302
Q

NOR

A

rare and polyagglutinable additon of alpha- 1-4 galactose to terminus of P (part of P1PK blood group 003)

303
Q

PX2 on Pk phenoype

A

Pk phenotypes are lacking PX2 antigen due to B3GALNT mutation

304
Q

FY6 FY3 FY5 which is resistant to enzymes

A

Fy6 is susceptible, FY3 and FY5 are resistant

305
Q

R2R2 lacks which antigen

A

hrS and hrb (both are negative on e negative cells)

306
Q

Percentage of population FYa negative

A

35%

307
Q

VS+ percentage

A

26-40% a.a.

308
Q

Dib is negative in….

A

Indians

309
Q

FY3 positive in

A

100% whites 32% blacks (either Fya or Fyb and 68% of blacks are Fya-Fyb-) FY5 IS THE SAME!!

310
Q

Which Fy antibody is negative when tested against Rh null cells

A

Fy5

311
Q

f percentage

A

65% positive in whites

312
Q

Ch/Rg enzymes

A

Sensitive to ficin/papain

313
Q

Gerbich enzymes

A

sensitive to ficin/papain

314
Q

CIS-AB

A

both A and B are inherited on one chromosme from a parent and O is inherited on the other. Weakly reacting A cells and B cells, B cells can exhibit MF agglutination, also contains a weak anti-B, reacts with all ordinary AB cells but not with cis-AB. High population found in Japan

315
Q

DIfference in structure of Rh antigens vs. ABH antigens

A

ABH-carbohydrates using enzyme to add sugar onto end, Rh antigen is on protein

316
Q

Fisher-Race Theory and nomenclature

A

3 different genes one each for Rh, C/c and E/e. Dce/DCe as example of how written

317
Q

Weiner theory and nomenclature

A

All Rh inherited together on single gene/allele. DCE for example. Nomenclature represents complete inherited haplotype: R1, R2 etc.

318
Q

Rh mod

A

weakened expression of all Rh antigens due to multiple mutations. partial suppression of Rh antigens due to a mutation within RHAG. LW expression also reduced. clinical symptoms similar to Rh null are present though less severe. S, s and U may also be depressed

319
Q

little r double bar

A

rr with an equal sign above it. This denotes a true null Rh through the inheritance of two Rh amorph alleles

320
Q

weiner nomenclature- hr’

A

c

321
Q

weiner nomenclature- hr’’

A

e

322
Q

Rho nomenclature

A

D

323
Q

Rosenfield nomenclature

A

numerical translation for antigen typing, for example D antigen is Rh1 C is RH2 E is RH3 c RH4 and e-RH5. Testing for presence of these antigens is translated as: 1,2,3,-4,-5 as an example if they are negative for both c and e but positive for the other antigens

324
Q

ISBT blood group number terminology

A

every antigen provided a six digit identification number the first three are the antigen blood group the last three are the antigen for example the first three of D are 004 and the last three 001: 004001

325
Q

Scientist credited for recognizing the correct two genes for Rh system

A

Tipppet

326
Q

Difference between RHAG and rh components

A

RHAG is a polypeptide that is glycosolated (contains sugar structures)

327
Q

Which Rh haplotypes contains the largest amount of D antigen on the surface of the red cell

A

R2R2 (besides the elevated D phenotypes)

328
Q

Which side of the membrane are the ends of the Rh antigen on, intracellular or extracellular

A

They are both intracellular ends NH2 and COOH

329
Q

D- can make which antibody

A

very important distinction this is not D negative, this is elevated D with no RHCE gene/antigens, they can make anti-RH17 or anti-Hr0. Antibody is directed against the entire protein from RHCE

330
Q

P blood group antigens are a receptor for which bacteria?

A

P-fimbriated uropathogenic E. Coli. (UTI). Pk is a receptor for shiga toxins and P is a receptor for Parvovirus B19

331
Q

D– cells have a decrease in what additional RBC protein

A

CD47 is combined with RHCE on it’s transport to the membrane, when lacking the rhce the CD47 expression is decreased.

332
Q

He

A

antigen 004006 of MNSs blood group, 3% of african americans less than .1% of other races

333
Q

Mia

A

Miltenburger antigen in MNSs blood group: 004007 less than 0.1% caucasians, up to 15% chinese population

334
Q

Enhanced Enzyme

A

Jka, Rh, Gil, Vel, P1, P, Pk, I/i, ABO, Lewis, Lutheran

335
Q

Destroyed by enzymes

A

M/N, S/s, Fya/b, Xga, Cartwright, Chido Rogers, Knops Indian JMH

336
Q

Antigens where a is more common than b

A

cartwritght, colton, LWa

337
Q

Destroyed by DTT

A

K, Lutheran, Cromer, Indian, Cartwright, Dombrock, Knops, JMH, LW, Scianna-weakened

338
Q

Susceptible to Glycine acid

A

Kell

339
Q

IgM antibodies: antigens

A

M/N Sda, Lua, P1, Lewis

SBB (31 decks)

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