[14] CHAPTER VI LESSON 2 Flashcards
*Named after the first antibody maker in a Venezuelan family.
Diego (010)
- Expressed on RBCs of newborns.
Diego (010)
*Named in 1956 for the first antibody maker and used the last letter “t” in the patient’s last name, which was Catwright.
Cartwright (011)
*Named after the first antibody maker
Scianna (013)
*The antigens are expressed on cord RBCs.
Scianna (013)
*Named for the first antibody maker, Mrs. Dombrock.
Dombrock (014)
22 antigens: Dia , Dib, Wra, Wrb and Wu/DISK and 17 low-prevalence antigens.
Diego (010)
Yta – high prevalence
Cartwright (011)
Ytb – low prevalence
Cartwright (011)
Xga and CD99
Xg (012)
7 antigens: SC:1, SC:2, SC:3, Sc4, Sc5 (STAR), Sc6 (SCER), Sc7 (SCAN)
Scianna (013)
Doa, Dob, Gya, Hy, Joa
Dombrock (014)
*Carried on Band 3 or also known as Red Cell anion exchanger (AE1) or solute carrier family-4.
Diego (010)
*Dia is rare in most populations but is polymorphic in people of Mongolian Ancestry.
Diego (010)
In South American Indians, the prevalence can be as high as 54%.
Diego (010)
*Anti-Wra is commonly found with other antibodies.
Diego (010)
*Resistant to enzyme treatment.
Diego (010)
Anion exchanger, member 1 (SLC4A1)
Diego (010)
*The Yt antigens are antithetical and represent an amino acid substitution on the glycosylphosphatidylinositol (GPI)-linked RBC glycoprotein acetylcholinesterase (AChE).
Cartwright (011)
*Variably sensitive to enzymes (Ficin and Papain)
Cartwright (011)
Sensitive to DTT
Cartwright (011)
*The antigens are developed at birth but are expressed more weakly on cord RBCs than on adult RBCs, and are absent from RBCs of people with PNH III.
Cartwright (011)
*Inherited on X chromosome; frequency varies with sex.
Xg (012)
*Sensitive to Ficin and Papain; Resistant to DTT treatment.
Xg (012)
*The SC gene is located on chromosome 1 at 1p34.
Scianna (013)
The product of the gene is a protein called erythroid membrane- associated protein.
Scianna (013)
*Resistant to Ficin and Papain; slightly weakened by DTT.
Scianna (013)
*The antigens are carried on a mono-ADP-ribosyltransferase 4 (ART4) attached to the RBC membrane by the GPI anchor.
Dombrock (014)
*Hy phenotype is found only in blacks
Dombrock (014)
anti-Doa and anti-Dob antibodies are rarely found as a single specificity.
Dombrock (014)
- Antigens are present on cord RBCs, but are absent from PNH III RBCs.
Dombrock (014)
Resistant to Ficin, Papain and Glycine Acid EDTA
Dombrock (014)
Sensitive to 0.2 M DTT treatment.
Dombrock (014)
Named after the first antibody maker Calton, but the tube was misread.
Colton (015)
Expressed on RBCs of newborns
Colton (015)
4 antigens: Coa, Cob, Co3, Co4
Colton (015)
The antigens are carried on an integral membrane protein aquaporin 1 (AQP1).
Colton (015)
Anti-Cob is rarely found as a single specificity
Colton (015)
Resistant to enzyme treatment.
Colton (015)
3 LW Antigens: LWa, LWab – highprevalence LWb- lowprevalence
Landsteiner-Wiener (016)
The structure that carries the LW antigens is a glycoprotein known as intracellular adhesion molecule 4 (ICAM-4), a membrane of the immunoglobulin superfamily.
Landsteiner-Wiener (016)
The LW antigens may be depressed during pregnancy and in some diseases, such as lymphoma and leukemia.
Landsteiner-Wiener (016)
Resistant to treatment with enzymes and Glycine Acid EDTA.
Landsteiner-Wiener (016)
*Named after the 2 antibody producers, Ch for Chido and Rg for Rodgers.
Chido/Rodgers (017)
are clinically insignificant for transfusion.
Anti-Ch and Anti-Rg
Ch, Rg
Chido/Rodgers (017)
Anti-Ch and Anti-Rg
Ch and Rg antigens are not intrinsic to the RBC membrane, they are on the fourth component of complement C4, and are adsorbed onto RBCs from plasma.
Chido/Rodgers (017)
Anti-Ch and Anti-Rg
Antigens are sensitive to enzymes and found in plasma; antibodies have HTLA characteristics.
Chido/Rodgers (017)
Anti-Ch and Anti-Rg
Destroyed by Ficin and Papain
Chido/Rodgers (017)
Anti-Ch and Anti-Rg
Resistant to treatment with DTT and Glycine Acid EDTA.
Chido/Rodgers (017)
Anti-Ch and Anti-Rg
The antigens are carried on sialoglycoprotein structures GPC and GPD.
Gerbich (020)
The Leach type is the Gerbich null phenotype (Ge: -2,-3,-4)
Gerbich (020)
All antigens except for Ge4 are sensitive to enzymes.
Gerbich (020)
Resistant to treatment with DTT and Glycine Acid EDTA.
Gerbich (020)
Ge2 and Ge4: Ficin and Papain Sensitive
Gerbich (020)
Ge3: Ficin Resistant
Gerbich (020)
Named after Mrs. Gerbich, the first antibody producer.
Gerbich (020)
Expressed at birth
Gerbich (020)
6 high prevalence antigen (Ge2, Ge3, Ge4, GEPL, GEAT and GETI)
Gerbich (020)
5 low prevalence antigen (Wb, Lsa, Ana, Dha, and GEIS)
Gerbich (020)
An antibody was found in a black prenatal patient, Mrs. Cromer, that reacted with all RBCs except her own and 2 siblings.
Cromer (021)
DAF is strongly expressed on placental tissue and will adsorb Cromer antibodies.
Cromer (021)
Cra, Tca, Tcb, Tcc, Dra, Esa, IFC, WESa, WESb, UMC
Cromer (021)
Antigen is also found in plasma
Cromer (021)
located on Decay Accelerating Factor (CD55).
Cromer (021)
Distributed in body fluids and on RBCs, WBCs, platelets and placental tissue.
Cromer (021)
PNH III RBC’s are deficient in DAF so they lack Cromer antigens.
Cromer (021)
The Cr(a-) phenotype is typically found in blacks and is not found in whites.
Cromer (021)
Resistant to treatment with Ficin and Papain and Glycine Acid EDTA
Cromer (021)
Destroyed by achymotrypsin
Cromer (021)
Weakened with DTT.
Cromer (021)
Named after the first antibody maker, Mrs. Knops.
Knops (022)
Antigens are weakly expressed on cord RBCs and weaken upon storage of adult RBCs.
Knops (022)
Kna, Knb, McCa, Sla, Yka
Knops (022)
Located on Complement Receptor 1
Knops (022)
are clinically insignificant and have weak & “nebulous” reactivity at the antiglobulin phase
Knops antibodies
they are not inhibited by plasma.
Knops antibodies
Antibody reactivity is enhanced with longer incubation (e.g., 1 hour at 37oC)
Knops (022)
The “Helgeson phenotype”- null
Knops (022)
Antigen depression in SLE, PNH, and AIDS
Knops (022)
antigens are weakened by ficin treatment
Knops (022)
antibodies have HTLA characteristics
Knops (022)
Weakened by treatment with Ficin and Papain
Knops (022)
Destroyed by DTT.
Knops (022)
Antigen: Resistant to Glycine Acid EDTA
Knops (022)
The Indian blood group system was named because the first In(a+) individuals were from India.
Indian (023)
Ina, Inb are weakly expressed on cord RBCs
Indian (023)
4 antigens: Ina, Inb and the other 2 high prevalence antigens
Indian (023)
Antibodies are usually IgG and reactive in the antiglobulin test.
Indian (023)
Do not bind the complement.
Indian (023)
The Ina antigen is more prevalent in Arab and Iranian populations with Ina and Inb antigen expression being depressed on the dominant type Lu(a-b-).
Indian (023)
Sensitive to treatment with Ficin and Papain, DTT
Indian (023)
Resistant to Glycine Acid EDTA.
Indian (023)
Named after the antibody maker, Mrs. Kobutso
Ok (024)
Oka is well developed on RBCs from newborns Oka, OKGV, OKVM
Ok (024)
The OK antigens are carried on CD147, a member of the immunoglobulin superfamily that mainly functions as receptors and adhesion molecules.
Ok (024)
Anti-Oka has not been reported to cause HDFN. *Resistant to enzyme treatment.
Ok (024)
Raph for the first patient to make the alloanti-MER2.
Raph (025)
The antigen name (MER2) is derived from monoclonal and Eleanor Roosevelt, the laboratory where the antibody was produced.
Raph (025)
It was shown that MER2 is located in CD151, a tetraspanin.
Raph (025)
MER2 is abundant in on platelets and is expressed on erythroid precursors of individuals with either MER2+ and MER2-RBCs.
Raph (025)
Resistant to treatment with ficin and Papain
Raph (025)
Sensitive to treatment with Trypsin, achymotrypsin, pronase, and AET.
Raph (025)
MER2
Raph (025)
Named after the first antibody maker John Milton Hagen
JMH (026)
Weakly expressed on cord RBCs
JMH (026)
JMH; JMH2-JMH6
JMH (026)
Autoanti-JMH is often found in elderly patients with absent or weak antigen expression
JMH (026)
antibodies have HTLA characteristics
JMH (026)
antigens are sensitive to enzymes and DTT
JMH (026)
JMH antibodies are generally considered clinically insignificant.
JMH (026)
Destroyed by treatment with Ficin, Papain and DTT
JMH (026)
Antigens: Resistant to treatment with Glycine Acid EDTA.
JMH (026)
is genetically discrete from all other blood group systems
Gill (029)
GIL
Gill (029)
The antigen is found on the glycerol transporter aquaporin 3 (AQP3).
Gill (029)
The GILnull phenotype results from a frameshift and a premature stop codon.
Gill (029)
Enhanced with Ficin, Papin treatment of RBCs.
Gill (029)
Antigens: Resistant to DTT and Glycine Acid EDTA
Gill (029)
Newest blood group system
RH-Associated glycoprotein (030)
The Rh associated glycoprotein (RhAg) does not have Rh blood group antigens.
RH-Associated glycoprotein (030)
Two antigens assigned to the RHAG system:
1. Duclos (RHAG1)
2. Ola (RHAG2) *DSLK (Duclos type)
RH-Associated glycoprotein (030)
RHAG4
RH-Associated glycoprotein (030)
Part of a blood group collection rather than a system.
Cost (Csa and Csb)
Named after the first antibody maker
Vel
Variable antigen expression on red cells
Vel
both IgG and IgM antibodies are associated with hemolytic reactions (in vitro hemolysis)
Vel
antibodies react best with enzyme treated red cells.
Vel
High prevalence antigen named for Sid, who was the head of maintenance department at the Lister Institute in London.
Sda
Not expressed on RBCs of newborns but is in their saliva, urine and meconium
Sda
Antigen found in guinea pig and human urine
Sda
antibodies are typically weak and agglutination is mixed field
Sda
reduction of Sda expression during pregnancy
Sda
The soluble form of Sda is Tamm Horsfall glycoprotein found in urine.
Sda
Reactivity is described as small, refractile (shiny) agglutinates in a sea of free RBCs.
Sda
Resistant to treatment with enzymes.
Sda
First described in the serum of a black woman named Mrs. Augustine.
Ata
The antigen is fully developed at birth.
Ata
The antibody is usually IgG, reactive in the antiglobulin test and has caused severe HTRs.
Ata
has caused severe severe HTRs and one reported cause of HDFN.
Anti- Ata
Resistant to treatment with enzymes.
Ata
High prevalence antigen
Jra
The antigen is fully developed at birth.
Jra
Resistant to treatment with enzymes.
Jra
is usually IgG.
Anti-Jra
Appreciating the unique characteristics of each blood group system is helpful in understanding the serologic and clinical features of the associated [?].
antibodies
With the exception of the ABO system, antibodies that are [?] are usually not clinically significant and react at room temperature, whereas antibodies that are [?] require the antiglobulin test and are clinically significant.
IgM
IgG
Clinically significant
ABO, Rh, Kell, Kidd; Duffy; S, s, and U, Lutheran (Lub)
Usually clinically insignificant
I, Lewis, M, N, P1, Lutheran (Lua)
IgM
Antigens
White
Black
Phase
Enzyme
Class
Comments
Kell
9
2
AHG
→
IgG
IgG
IgG
IgG
lgG
IgG
Antigens in the Kell system
k
99.9
99.8
AHG
→
are destroyed by DTT
Кр°
2
<1
AHG
→
Kph
99.9
>99.9
AHG
→
Js*
20
AHG
Jsb
>99.9
99
AHG
Duffy
Fy*
66
10
AHG
IgG
Fy（a-b-） is protective
against malaria
Fyb
83
23
AHG
IgG
Kidd
Jk°
77
91
AHG
IgG
Associated with delayed transfusion reactions
Jk’
73
49
AHG
IgG
Lutheran
Lu*
7.6
5.3
RT
→
IgM
May exhibit mixed-field reactions
Lu’
99.8
99.9
AHG
→
IgG
Lewis
22
23
RT
IgM
Lewis antigens are found in plasma and red cells
72
55
RT
↑
IgM
Le” arises from H, Le, and Se genes
> 99.9
99.9
RT
IgM
Frequently found as a cold autoantibody
P1PK
<1
RT
IgM
I is negative on cord cells
P1
79
94
RT
IgM
MNS
78
74
RT
IgM
Antigens M and N show dosage
N
72
75
RT
S-s- are also U-negativ-
55
31
AHG
var
IgG
89
93
AHG
var
IgG
9
2
AHG
IgG
K
99.9
99.8
AHG
IgG
k
2
<1
AHG
IgG
Кpa
99.9
>99.9
AHG
IgG
Kpb
<1
20
AHG
IgG
Jsa
> 99.9
99
AHG
IgG
Jsb
66
10
AHG
IgG
Fya
83
23
AHG
IgG
Fyb
77
91
AHG
IgG
Jka
73
49
AHG
IgG
Jkb
7.6
5.3
RT
→
IgM
Lua
99.8
99.9
AHG
IgG
Lub
22
23
RT
IgM
Lea
72
55
RT
个
IgM
Leb
> 99.9
99.9
RT
IgM
I
<1
<1
RT
IgM
i
79
94
RT
IgM
P1
78
74
RT
IgM
M
72
75
RT
IgM
N
55
31
AHG
var
IgG
S
89
93
AHG
var
IgG
s
Antigens in the Kell system are destroyed by DTT
Kell
Fy(a-b-) is protective against malaria
Duffy
Associated with delayed transfusion reactions
Kidd
May exhibit mixed-field reactions
Lutheran
are found in plasma and red cells
Lewis antigens
arises from H, Le, and Se genes
Leb
Frequently found as a cold autoantibody
I
is negative on cord cells
I
show dosage
Antigens M and N
are also U-negative
S-s-
