antigen/antibody features

Rh

only on RBCs

IgG, very immunogenic

shortened RBC lifespan, anemia

resist/enhanced by enzymes

LW

strong reaction w/ all cord cells

destroyed by thiols

mistaken for anti-D

Kell

very antigenic

RBC, BM, lymph tissue, fetal cells

unaffected by enzymes, destroyed by thiols

most common AB in pretransfusion testing

delayed transfusion reaction

Duffy

AGs most important in routine blood bank

2 AGs destroyed by enzymes, 3 not

common phenotype does not make AB bc AG still in tissues

secondary AB

Kidd

on RBCs and kidney endotheolium

delayed transfusion reactions

dosage

binds complement, in vitro hemolysis

ABs degrade in storage

MNS

4 AGs destroyed by enzymes, all by thiols

dosage

1 AB seen in children, bac inf

P1PK P Glob

precursor antigen

AG degrades during storage

common in Asians

universal AB in null phenotype

1 AB can be neutralized w/ substance

1 AB binds complement, in vitro hemolysis

1 AB biphasic, in children w/ viral inf

Lutheran

poorly dev at birth, not on cord cells

1 AB mixed field agglu

can’t cause HDFN

AG degrades during storage

Lewis

AGs from plasma attach to RBCS, not on cord cells

neutralized by substance

enhanced by enzymes

ABs have broad thermal range and degrade during storage

bind complement, in vitro hemolysis

HTLA

high frequency AGs

weak, persistant reactions

neutralized by human serum

AGs degrade during storage

I

carbohydrate AGs

on cord cells then change at 2 years

most common cold autoAB

assoc w M. pneumonia and malignancies