Some are reactive at Room temperature and binds complement at 37°C (detectable in AHG phase)
Associated with Fascioliasis, Clonorchis and Opisthorchis viverinii infection
Anti-PP1 Pk (P blood group) is originally called as anti-Tja; first described on serum of Mrs. Jay (has p phenotype with adenocarcinoma of stomach)
Tumors contained P system Antigens and the Ab has cytotoxic properties that may have helped prevent metastatic growth post surgery
Produced by all p individuals without exposure
Reacts with all RBCs except from p individuals
Components are separable through adsorption
Have IgM and IgG component
Have a wide thermal range and binds complement (potent hemolysin)
Can cause HTR and HDN
Associated with spontaneous abortion in early pregnancy
Alloanti-P are naturally occurring alloantibody in sera of all p k individuals
Reactivity is similar to anti-PP1 Pk (potent hemolysin)
Reacts with all RBCs except auto control and p phenotype
Autoanti-P (P blood group) is associated with Paroxysmal Code Hemoglobinuria
Cold-reactive antibody
IgG with biophasic property
Binds RBCs in the cold (4°C) and causes hemolysis (complement activation) at 37°C
Demonstrated by Donath-Landsteiner test
Paroxysmal nocturnal Hemoglobinuria is associated with acquired somatic mutations in a Pa gene resulting in deficiency in the key accelerating factor and MIRL protein in RBC leading to susceptibility to complement mediated lysis
Paroxysmal code Hemoglobinuria is associated with the formation of autoantibodies that has an affinity in the P antigen and this autoantibody demonstrate biphasic property
Biphasic property is when at 4°C, the autoantibodies binds to red blood, when warm temperatures, these bound antibodies will now cause hemolysis
Autoanti-pk (P blood group) is seen in serum of individuals with biliary cirrhosis and AHA; inhibited by hydatid cyst fluid
Tippett et al in 1965, described an antibody in serum of Hodgkin lymphoma patients, the Luke antigen
I blood group system is discovered by Wiener et al in 1956
Only has 1 antigen
I and i antigen (I blood group) are high incidence antigens (90% of the community has it)
Expressed in reciprocal relationship (developmentally regulated)
Enzyme treatment of RBCs enhances I/i antigens
i antigen = predominant in fetal RBCs, decreases during the first 18 months of life
I antigen = increases until adult proportion are reached
Anti-I (I blood group) are weak, naturally occurring IgM
Common autoantibody (particularly for those infected with Mycoplasma pneumoniae)
Testing at 4°C and enzyme treatment of RBCs may be required
Strong agglutination with adult RBCs and weak to no agglutination with cord RBCs(I blood group)
Pathologic Anti-I (I blood group) is associated with cold agglutinin disease (strong IgM with broad thermal range of activity)
Can cause autoagglutination, vascular occlusion or hemolytic anemia
Production may be stimulated by Mycoplasma pneumoniae infection (I-like antigen)
Not associated with HDN
Anti-i (I blood group) are cold reacting and rare; it produces strong reaction with cord RBCs and adult i RBCs
Weaker reactions with adult I RBCs
IgM, reacts best at 4°C, saline suspended cells
Associated with infectious mononucleosis, myeloid leukemia and alcoholic cirrhosis
Anti-IT (I blood group) is IgM and frequently found in Melanesians and Yanomama Indians in Venezuela; associated with Hodgkin’s lymphoma
Kell blood group system has 24 high and low incidence antigens; it is the first blood group system discovered after the introduction of AHG testing
Anti-K (Kell blood group) is discovered from serum of Mrs. Kellager in 1946
Levine et al in 1949, discovered anti-k, which has high incidence antithetical partner of K