Antigen/Antibodies other an ABO Flashcards
Antibodies that react at the RT phase
P, I, H, Lewis
M, N,
Lutheran(a)
Antibodies that react at AHG phase
S, s, U, Kell
Duff, Kidd
Lutheran (b), Xga
Rh, rarely lewis
5 phenotypes of P system
P1, P2, p, P1k, P2k
Detectable antigens for P1
P1P
Detectable antigens for P2
PP
Detectable antigens for p
None
Detectable antigens for P1k
P1Pk
Detectable antigens for P2k
PkPk
Antibody that can be inhibited by hydatid cyst fluid
Anti-P1
Antibody/antibody class associated with paroxysmal cold hemoglobinuria
Auto anti-P
IgG biphasic
ID by Donath-Landsteiner test
What antigen in the P system deteriorates rapidly during storage?
P1 antigen
What is the Donath-Lansteiner test used for?
Anti-P autoantibody
- No gene for I or i but the presence or absence of many glycosyl transferases results in different sequences added to the original structure
- I and i antigens are the subterminal portions of the molecules that are eventually converted to H, A, or B
Transition of i to I antigen
Antibody characteristics of Ii system
IgM - only significant if it is masking the presence of another antibody. Not RBC stimulated, usually autoantibody
Transient antibody associated with infectious mononucleosis
Anti-i
Anti-I thermal activity
usually weak IgM
Potent anti-I thermal activity
Can occur with an IgM molecule that has a wide thermal range - reacting at 30 C or warmer.
Anti-i
Usually IgM and react best at 4 C
Antibody associated with Mycoplasma infections
Anti-I (cold agglutinin disease)
Anti-I cord blood activity
Does NOT agglutinate with cord cells
Anti-i cord blood activity
Agglutinates with cord blood
How can you differentiate pathogenic anti-I and non pathogenic anti-I?
Pathogenic anti-I will react equally with adult or cord cells (ii)
Which blood group is most likely to make anti-H?
A1B combination because they have the least amount of H on the surface
Acquisition of Le (a)
Substance is produced if the individual has inherited the Le gene. This substance will absorb onto the surface of the RBC & become an RBC surface antigen & is a glycolipid Le (a+b-)
Acquisition of Le (b)
Substance is interaction of the Le gene, the H gene, & the Se gene. If all three are present, the Le (b) soluble antigen is produced in addition to Le (a) when both are in secretions.
- More successful at absorbing onto the surface of RBC
- Le (a-b+)
Is Le (a+b-) a secretor?
No
Is Le (a-b+) a secretor?
Yes
Is Le (a-b-) a secretor?
Unkown
Do enzymes affect the Lewis antigen?
Yes, by enhancing the activity
Where are the Lewis antigens produced?
Tissue
Significance of anti-Le(a), anti-Le(b)
Considered insignificant because of their neutralization by Lewis substances, poor attachment to RBC, IgM class
Do the Lewis antigens show dosage and are the reactions changed with enzymes?
No dosage, reactions are enhanced by enzymes
Who is most likely to make anti-Le(a) or Le(b)?
Pregnant women sometimes change to Le(a-b-) no matter what Lewis genes they have inherited.
Chromosome MNSsU is on
4
Does MNSsU show dosage?
Yes
Enzyme reaction of MNSsU system
All decrease with enzymes
When MNSsU system is developed
At birth
Precursor to MN
Glycophorin A
Precursor to SsU
Glycophorin B
Anti-M antibody Class
Naturally occurring IgM or rarely immune IgG
Anti-M complement fixation
Does not fix complement
Anti-M temp of reactivity
Not reaction above or at 30 C - not clinically significant
Anti-M cause of HDN/HTR
Should be concerned about HDN
Is anti-M RBC stimulated?
No
Anti-N antibody class
IgM or occasional IgG
Does anti-N fix complement?
Does not fix complement
Anti-N temp of reactivity
Only significant if reacting at or above 30 degrees
Does anti-N have the ability to cause HDN/HTR?
No
Is anti-N RBC stimulated?
No
En(a-) pheotype
Individuals make anti-En(a)
Appears to be antibody to various portions of glycophorin A
M(k) phenotype
Silent gene, no M, N, S or s
Anti-S antibody class
IgG, occasionally IgM
Does anti-S fix complement?
Poorly
Anti-S temp of reactivity
usually 37 degrees and AHG phase
Does anti-S have the ability to cause HDN/HTR?
Yes
Is anti-S RBC stimulated?
yes
Anti-s antibody class
IgG
Can anti-s fix complement?
poorly
Anti-s temp of reactivity
Usually 37 degrees and at AHG phase
Does anti-s have the ability to cause HDN/HTR?
Yes
Is anti-s RBC stimulated?
yes
What is the prevalence of the U antigen if S and s antigen is negative?
U is part of the S structure, so if no S or s, then no U
Kell system dosage
Occasional
When is the Kell system developed?
It is well developed at birth
How do enzymes affect the Kell system?
No change, but will decrease with AET & ZZAP
McLeod phenotype & syndrome
Rare, lacks K(x) & K(m), x-linked
Patients have a variety of muscle and nerve disorders
Anti-K antibody class
IgG
Can anti-K fix complement?
Yes, sometimes
Anti-K temp of reactivity
AHG phase
Does anti-K have the ability to cause HDN/HTR?
yes
Is anti-K RBC stimulated?
Yes
Rare antibodies of the Kell system
Kp(a), Js(a), k, Kp(b), Js(b)
How antigenic are the Kell antigens?
Very antigenic
Why don’t we see anything other than anti-K very much in the Kell system?
Antigens are either very high frequency or very low frequency so exposure to an antigen that is foreign would be rare
Does the Duffy system have dosage?
Yes
When is the Duffy system developed?
At birth
How does enzymes affect the Duffy system?
It decreases the reactivity
Which antigen has a relationship to the Rh blood group?
Fy(6)
Duffy system antibody clas
IgG
Can duffy system antibodies fix complement?
Can bind compliment but not usually to lysis
Duffy system antibody temp of reactivity
AHG phase
Does the Duffy system antibodies have the ability to cause HDN/HTR?
yes
Are the Duffy system antibodies RBC stimulated?
yes
What is the antigen inheritance and significance of Fy(a-b-) in the black population?
68% of blacks will inherit. This allows them to resist Plasmodium vivax.
Describe Fy(x) antigen and antibody
Antigen: weak form of Fy(b)
Antibody: none
Describe Fy3 antigen and antibody
Antigen: probably part of the Fya and/or Fyb structure
Antibody: Seen most often in blacks that are Fy(a-b-)
Describe Fy5 antigen and antibody
Antigen: not entire understood but different than Fy3. There is interaction between Rh and Duffy glycoprotein
Antibody: Reacts with Fy(a-b-)Fy3- cells
Kidd System antibody class
IgG
Can the Kidd system fix complement?
It binds compliment well
Kidd system temp of reactivity
AHG phase
Does the Kidd system have the ability to cause HDN/HTR?
Yes
Is the Kidd system RBC stimulated?
Yes
Why are the kidd antibodies particularly problematic?
Anti-Jk(a) and anti-Jk(b) quantity fade quickly from circulation and if stimulated, may make an anamnestic response with delayed intravascular & extravascular hemolysis
Do Kidd antigens have dosage?
Yes
When are Kidd antigens developed?
By birth
What affect does enzymes have on Kidd antigens?
Increased activity
Does Lutheran antigens have dosage?
Yes
When are Lutherans antigens developed?
Poor at birth
How are Lutheran antigens affected by enzymes?
No effect
Anti-Lu(a) antibody class
IgM, and rare IgG
Does Anti-Lu(a) fix complement?
Will bind compliment but not to lysis
Anti-Lu(a) temp of reactivity
RT
Does Anti-Lu(a) have the ability to cause HDN/HTR?
Not usually but can be mild
Is Anti-Lu(a) RBC stimulated
No
Anti-Lu(b) antibody class
IgM/IgG
Does Anti-Lu(b) fix complement?
Occasionally
Anti-Lu(b) temp of reactivity
37/AGH phase
Does Anti-Lu(b) have the ability to cause HDN/HTR?
Yes but very mild
Is Anti-Lu(b) RBC stimulated?
Yes
2 non-RBC stimulated antibodies that may occur in Rh group
Anti-Cw
Anti-E
Xg(a) chromosome location
X chromosome
Xg(a) antigen genetics
Only blood group that is produced from a gene on the X chromosome
Anti-Xg(a) antibody charactersitics
IgG - AHG phase reactivity Can bind complement but not to hemolysis Not implicated in HDN/HTR Destroyed by enzymes Rare
What is the Bg antigen
Residual MHC I on RBC surface
Define High Titer Low Avidity Antibodies (HTLA)
High titer (>64) reactivity but low avidity for agglutination when binding to its antigen (weak reactions)
Characteristics of HTLA antibodies
IgG AHG phase Usual titer > 64 Poor agglutination response with corresponding antigen Clinically insignificant React poorly with LISS
Antigens that are defined as HTLA
Chido, Rodgers, Knops, McCoy, York, Cost
What is unique about Chido and Rodgers antibodies?
Can be neutralized or inhibited by plasma containing C4d
