5 Other Major Blood Group Systems

Cards (73)

  • MNS blood group system is composed of 43 antigens
    • Landsteiner and Levine immunized rabbits with human RBCs
    • Anti-M and Anti-N were reported (1927)
    • M and N-antithetical antigens
    • Wash and Montgomery discovered S antigen
    • In 1951, s antigen was discovered
    • Wiener discovered U antigen
  • M and N Antigens (MNS blood group) are found on glycophorin A that is found in the surface of RBC
    • Well developed at birth
    • Easily destroyed by enzymes ficin, papain, bromelin, trypsin and pronase
    • Also destroyed *ZZAP (Dithiothreitol (DTT) + ficin/papain)
    • Not affected by DTT alone
  • S and s antigens (MNS blood group) are located on a smaller glycoprotein → Gycophorin B
    • Differentiated by the amino acid 29th position
    • S – methionine
    • s - threonine
    • Well developed at birth
    • Less easily degraded by enzymes
    • Destroyed by ficin, papain, bromelin, pronase and chymotrypsin
  • Anti-M (MNS blood group) is a naturally occurring saline agglutinin (can occur without exposure to antigen)
    • Reacts at <37°C
    • 50-80% are IgG
    • Do not bind complement regardless of Ab class
    • Do not react with enzyme-treated cells
    • Reacts better with MM genotypes than with MN genotypes
    • Some reacts best at pH 6.5
    • Some may react only to RBCs exposed to glucose
    • Clinically insignificant as long it does not react at 37°C
    • Rarely causes HTR or HDN
  • Anti-N are cold-reactive IgM or IgG saline agglutinin (MNS blood group)
    • Does not bind complement
    • Does not react with enzyme-treated cells because they are easily destroyed by enzymes
    • Demonstrate dosage effect
    • Clinically insignificant unless reactive at 37°C
    • Implicated in rare cases of HDN
    • Also seen in renal patients who are dialyzed on equipment sterilized by formaldehyde
  • Dosage effect is the phenomenon wherein your antibodies react stronger in homozygous RBCs than heterozygous blood cells
  • Damage of M and N antigen due to exposure to formaldehyde produces the anti-Nf antibodies
    • associated with rejection of chilled transplanted kidneys
  • Anti-S and Anti-s (MNS blood group) are clinically significant
    • IgG, reactive at 37°C and AHG phase
    • Demonstrate dosage effect
    • May or may not react with enzyme-treated cells (less destroyed by enzymes)
    • More significant compared to anti M and anti N
    • May bind complement and have been implicated in severe HTR and HDN
  • MNS system is found on chromosome 4
  • Anti-M lectin:
    • Iberis amara → causes agglutination when mixed with RBC
  • Anti-N lectins:
    • Bauhinia variegata
    • Bauhinia purpurea
    • Vicea graminea
  • U phenotype is a universal antigen, located on GPB (MNS blood group)
    • High incidence antigen (>90% in population)
  • Anti-U (MNS blood group) is produced by individuals who lack GPB and IgG; has been reported to cause HTR and HDN
  • GPA may serve as receptor for certain pyelonephrogenic strain of Escherichia coli
  • GPA, GPB, GPC may serve as receptors for P. falciparum
  • P blood group system is composed of P, P1 , Pk , Luke*
    • It cannot be considered as a single blood group
    • At least 2 biosynthetic pathways and genes located at different loci
    • Phenotypes: P+ and P-
    • Additional phenotypes: P1 k and P2 k
  • Landsteiner and Levine injected human RBCs to Rabbits in 1927, and produced the anti-P
  • Levine in 1951, described anti-Tja (anti-PP1 Pk), which is produced by P null individuals
  • Matson et al in 1959, described pk, which is expressed in all RBCs except in p phenotype
  • P1 Antigen (P blood group) is found on fetal RBCs during 12 weeks but weakens with gestational age
    • Poorly expressed at birth and fully expressed at 7 years
    • Deteriorates rapidly on storage
  • Anti-P1 (P blood group) are IgM, naturally occurring P1 (-) individuals
    • Weak, cold-reactive saline agglutinin (4°C)
    • 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