Other Antigens

Front 1

-What type of inheritance are the Lu antigens?
-Are they immunogenic?
-How developed at birth?

Back 1

-Co-dominant; expression varies
-No; not very immunogenic.
-Poorly developed at birth.

Front 2

What type of antibodies are Anti-Lua?

Back 2

-Nat'ly occurring IgA, M, or G.

Front 3

What temp is optimal for Lua?
Does it bind complement?
Enzyme response?

Back 3

-Usually roomtemp; rare warm.
-Occasionally binds complement.
-Enzymes make reactivity variab.

Front 4

How frequent is LuA as a Ag?
Does it cause HDR/HTN?

Back 4

Low frequency.
No, does not cause HTR; may cause mild HDN if IgG.

Front 5

What's the diffnc betwenn LuA and LuB?

Back 5

LuB is significant, warm-rctv, IgG.

Front 6

What type of antibodies are Anti-LuB?

Back 6

Immune or Naturally occurring IgA, M, or G.

Front 7

What temp is optimal for LuB?
Does it bind complement?
Enzyme response?

Back 7

37, Warm.
Occasionally binds complement.
-Enzymes make reactivity variab.

Front 8

Does Anti-LuB cause HDN/HTR?

Back 8

MAy cause either.

Front 9

What are the duffy antigens?

Back 9

Fya and Fyb

Front 10

-What type of inheritance are the duffy antigens?
-How immunogenic are they?
-How developed at birth?

Back 10

Codominant.
Poor immunogens.
Well developed.

Front 11

How many alleles do we know about for duffy antigens?
What are they?

Back 11

Four:
Fya, Fyb, Fy, and Fyx.

Front 12

What is Fy?
What population is it seen in, and why?

Back 12

the third allele that codes for the absence of Fya or Fyb.
Seen in blacks, a natural defense against malaria.

Front 13

What is Fyx?

Back 13

Variant gene that encodes weakened Fyb antigen.

Front 14

What temp optimal for Anti-Fya?
Does it bind complement?
Enzyme response?

Back 14

Warm, IgG.
Yes; activates complement.
Won't react - enzyme destroys these antigens.

Front 15

Does Fya show dosage?
Does it cause HDN/HTR?

Back 15

Yes.
Yes.

Front 16

How does Fyb compare to Fya?

Back 16

Pretty similar, but very rare and often found with Anti-K and Anti-c

Front 17

In whom would you find Fya3, 4, or 5?

Back 17

Blacks with phenotype Fya-b-

Front 18

How many and what antigens are in the Kell Blood Group system?

Back 18

Six: K, k, Kpa, Kpb, Jsa, Jsb.
(1,2,3,4,6,7)

Front 19

Of all the kell antigens, which is most frequent?

Back 19

K

Front 20

How are Kell antigens inherited?
How developed at birth?

Back 20

-Inherited as spcfc haplotypes, gene complex. Codominant.
-Well developd at birth.

Front 21

What are the haplotypes inherited, what's more common?

Back 21

K/k, Jsa/Jsb, Kpa/Kpb.

k/Jsb/Kpb is much more common than K/Jsa/Kpa.

Front 22

What are the frequencies of:
Kpa
Kpb
Jsa
K
Ko

Back 22

Kpa = rare, in blacks
Kpb = common in both
Jsa = common in blacks, rare in whites.
K = neg in 90% of population.
Ko = very rare, kell null

Front 23

What is the most common Kell haplotype?

Back 23

k/Jsb/Kpb

Front 24

What situates kell antigens on the RBC?
what cells lack it?
what phenotypes is it diminished in?

Back 24

-a 93-kD protein.
-Ko, null cells.
-McLeod

Front 25

What is Kx?

Back 25

Not part of the Kell glycoprotein; stabilizes RBC membrane/cytoskeleton.

Front 26

Who is missing Kx, and what is the result?

Back 26

McLeod phenotypes; results in membrane defects, problems.

Front 27

What are the 2 diseases associated with Kell null cells?

Back 27

-McLeod Phenotypes
-Chronic Granulomatous Disease

Front 28

What causes Chronic Granulomat. disease?

Back 28

The lack of Kx antigen on WBCs. Result: defective WBC function.

Front 29

Quick: you see a chronic bacterial infection; what do you think?

Back 29

Check for absence of Kx antgen, may be chr. granulamatous dises.

Front 30

What type of Ab are Kell?
Are they immunogenic?

Back 30

-Natural OR Immune occuring, usually IgG (IgM is rare).
-YES! these antigens rate second only to D in immunogenicity!

Front 31

Should we care about Kell antibodies?

Back 31

YES! they are 2/3 of the non-Rh antibodies we'll see in labs.

Front 32

What temp do Kell abs react at?
Do they show dosage?
Do they cause HDN/HTR?

Back 32

Warm - AHG.
Yes, occasionally.
Yes.

Front 33

How often would you see Anti-k, and why?

Back 33

VERY rarely, because only .2% is K/K, able to make the antibody.

Front 34

How do you normally detect anti-Kpa or anti-Jsa?

Back 34

With incompatible donor screens, because these rare antigens not typically on screen cells.

Front 35

What on earth is the Xg blood group system?
What are the alleles?

Back 35

The sex linked system :)

Xga/Xg
(Xg is amorphic)

Front 36

Who is the Xga gene more frequently found in?

Back 36

Females -> 89%

Males -> 66%

Front 37

If an Xga pos male mated with an Xg female, what would result?

Back 37

All neg males (Xg)
All pos females (Xga)

Front 38

Anti-Xga characteristics:
-Type? How stimulated?
-Optimal reaction at?
-Complement? enzymes?
-HTR/HDN?

Back 38

-IgG, immune stimulated.
-Reacts at warm better than IAT.
-May bind complement. Enzymes depress it.
-Maybe HTR, NOT HDN.

Front 39

What holds the MNSs antigens onto RBCs?

Back 39

Glycoproteins
GPA for M/N
GPB for S/s

Front 40

Do enzymes alter MN antigens?
Which enzymes?
How are MN antigens inherited?
Do they show dosage?

Back 40

Yes; destroys them.
Ficin trypsin and papain.
Codominant; show dosage

Front 41

How developed at birth are M/N?
Are they only on RBCs or other?

Back 41

-Well; 9 wks post-birth.
-Also on renal tissue.

Front 42

What phenotype denotes M/N neg cells?

Back 42

En(a-) --> represents the 2 En genes encoding GPA negative.

Front 43

-How do Ss antigens respond to enzymes?
-How often does U occur?

Back 43

-Variably inhibited by FICIN and papain.
-U is high incident.

Front 44

what is unique about U- and U variant cells?

Back 44

Lack the 'N' antigen, GPB; so are S-s-U-.
This is seen only in blacks.

Front 45

What type of Ab is Anti-M?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?

Back 45

-Usually IgM, maybe IgG.
-Optimal at R.T. if IgM.
-Does NOT activate complement.
-Shows dosage.

Front 46

What enhances some Anti-M's?
What destroys them?
Does Anti-M cause HDN/HTR?

Back 46

-Enhance w/ acid environment.
-Destroy with enzymes.
-RARE cause HDN/HTR

Front 47

What type of Ab is Anti-N?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?

Back 47

-Naturally occuring, IgM.
-Optimal is R.T.
-Does not activate complement.
-Shows dosage.

Front 48

What destroys Anti-N?
Does Anti-N cause HDN/HTR?
Is it clinically significant?

Back 48

-Enzymes destroy
-Rare cause of HDN/HTR.
-Only if reacts at 37.

Front 49

What type of Ab is Anti-S?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?

Back 49

-Immune, IgG!!
-Coomb's phase.
-YES
-It may

Front 50

-How does Anti-S react to enzymes?
-Does it cause HTR/HDN?

Back 50

Variably.
Yes.

Front 51

How does anti-s compare to Anti-S?

Back 51

-Also immune IgG, but rarer.
-

Front 52

What type of Ab is Anti-U?
What optimal temp does it react?
Does it activate complement?

Back 52

-A rare immune IgG.
-Coomb's phase.
-Yes.

Front 53

-How does Anti-U react to enzymes?
-Does it cause HTR/HDN?
-What type of blood crossmatch?

Back 53

-Enzymes HAVE NO EFFECT!
-Yes.
-S-s-U- from blacks.

Front 54

What antigens are in the Kidd blood group system?
How developed are they at birth?

Back 54

-Jka and Jkb.
-Well developed.

Front 55

What type of inheritence is in the Kidd group?

Back 55

Codominant.

Front 56

What type of Ab are anti-Jka/b?
What optimal temp does it react?
Does it activate complement?
How immunogenic are the rxns?

Back 56

Immune, IgG.
Coomb's.
Yes.
Weak reactions.

Front 57

-How can you enhance Kidd group reactions?
-Do the antibodies show dosage?

Back 57

-By using enzyme-treated RBCs.
-Yes.

Front 58

What spcfc type of IgG are the Kidd antibodies?
how does it alter their rxtns?

Back 58

IgG-3
-Makes them "notorious" for delayed HTR.