MAJOR BLOOD GROUP SYSTEM

• MN antigens • found in glycophorin A; • M and N antigens differ in their amino acid residues at positions 1 and 5. • M has serine and glycine; N has leucine and glutamic acid • Exhibits dosage effect • Destroyed by enzyme treatment and ZZAP+DTT+ papain/ ficin
• Ss antigens • Found in glycophorin B; S has methionine; s has threonine
• Anti-M • Naturally occurring , saline agglutinations; cold reactive, IgM in nature; react best at pH 6.5. • Anti-M lectin include: Iberis amara
• Anti-S and Anti-s • often IgG in nature, reactive at 37 degree celcius
• U phenotype • U= universal • Anti- U is formed by S-s- individuals, usually of black origin (African black)
• “I “ BLOOD GROUP SYSTEM 1. I =“ individuality” • I antigen is found adults; Infants are rich in I antigen • Can be neutralized by human milk • I activity is increased in individuals with Bombay phenotype and if ABH sugars are removed by enzymes
• Phatogenic autoanti-I • associated with cold agglutinin syndrome, especially in cases of Primary atypical Pneumonia ( Mycoplasma pneumonia)
• Anti-I • Associated with infectious mononucleosis (caused by Epstein Barr virus)
• P1 antigen • deteriorates rapidly on storage
• Anti- P1 • naturally occurring IgM; weak , cold reactive saline agglutinin • Can be neutralized using hydatid cyst fluid from Echinococcus granulosus infection, pigeon droppings or turtle dove egg white.
• Anti-Tja (anti-PP1Pk) • First described in serum of a patient with adenocarcinoma (tumor) of the stomach, • Associated with increased incidence of spontaneous abortions in early pregnancy
• Autoanti-P • Associated with PCH (paroxysmal cold hemoglobinuria) Bind RBCs in the cold and, via complement activation, the coated RBCs lyse as they are warmed to 37C • An IgG autoantibody described as a biphasic hemolysin. • Demonstrated by the Donath-Landsteiner Test
• Disease associations • P antigens can be associated with pyelonephritogenic E.coli, Streptococcus suis, Shigella dystenteriae, Vibrio cholerae, V. parahaemolyticus • Receptor for parvovirus B19 • Parasitic infectious are associated with anti-P1
• KELL BLOOD GROUP SYSTEM • Originated from Mrs. Kellaher, from whom anti-K was first identified • Second rated to D in terms of immunogenicity • Production is coded by the KEL gene located on chromosome 7 • Anti-K are usually IgG, reactive in AHG phase, Implicated in HDN and HTR
• McLeod phenotype - X-linked inheritance, males are affected - RBCs are acanthocytic in nature - WBCs of patient are deficient in enzyme NADH-oxidase - associated with CGD (Chronic Granulomatous Disease) - RBCs lack Kx and Km and marked depression of all other Kell antigens.
• DUFFY BLOOD GROUP SYSTEM • Duffy null (Fy a-b-) phenotype is associated with African-American population and it confers resistance against Plasmodium vivax infections. • Fya and Fyb antigens do not store well in saline suspension • Fya and Fyb antigens are destroyed by enzymes treatment • Anti-Fya and anti-Fyb are usually IgG, best react at the antiglobulin phase • Anti-Fy3 is an antibody made by Duffy null phenotype
• Kidd blood group system • Kidd antibodies have NOTORIUS REPUTATION in blood bank due to its association to delayed hemolytic transfusion reaction • Demonstrate dosage; enhanced by enzymes treatment; usually IgG, warm reactive. • Antibodies are labile on storage • Jk(a-b-) or jk null phenotype RBCs resist lysis in 2M urea • Anti- jk-3 is produced by individuals with the Kidd null phenotype • Organisms with jkb-like specificity include Enterococcus faecium, Micrococcus and Proteus mirabilis
• LUTHERAN BLOOD GROUP SYSTEM • Named from the misinterpretation of the blood donor’s name, Luteran, where the antibody was first identified • Anti- Lua reacts well with saline, can produce mixed-field agglutination; thermal optimum is 12-23C • Anti-Lub is an incomplete antibody, reacts better in AHG phase • Lu(a-b-) results from either amorphic gene (Lu, recessive type0 where is no Lu antigen production; or inhibitor gene (InLu, dominant type0 where Lu antigen synthesis is suppressed.