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Other Blood Group Systems

Other Blood Group Systems. Introduction. For each blood group system you MUST know : Antigen development, if important. Antibody class usually involved. Phase of reactivity in in-vitro tests. Clinical significance. Whether donor units must be antigen negative.

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Other Blood Group Systems

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  1. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  2. Other Blood Group Systems

  3. Introduction • For each blood group system you MUST know: • Antigen development, if important. • Antibody class usually involved. • Phase of reactivity in in-vitro tests. • Clinical significance. • Whether donor units must be antigen negative. • Any unique characteristics of the blood group antigens and/or antibodies. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  4. Major Blood Group Systems • Lewis • I • P • MNSs • Kell • Kidd • Duffy BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  5. Systems that Produce Cold-Reacting Antibodies

  6. Lewis System (ISBT 007) • Major antigens Lea and Leb , they are glycoproteins • Antigens ARE NOTintrinsic to RBCs but are absorbed from the plasma and inserted into RBC membrane. • Genetic control reside in single gene “Le” • Amorph le, if homozygous will not have Lewis antigens • Lea formed first, then modified to form Leb • Lewis phenotype of RBC can be changed by incubating with plasma containing Lea or Lebglycoplipid. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  7. Lewis System • Lewis antigens in infants • Antigens absent or extremely weak at birth • Expression of Leb is gradual • Birth Le (a-b-) • 2 months Le(a+b-) • 12 to 18 months Le(a+b+) • 2 to 3 years Le (a-b+) • Lewis antigens cannot be used for paternity testing on infants. Why? BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  8. Lewis Antigens and Pregnancy • Antigen strength may decline dramatically during pregnancy. • Transiently Le (a-b-) may produce Lewis antibodies during pregnancy. • Antigens return after delivery and antibodies disappear. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  9. Interaction of Le, Se and H Genes • The le, h and se genes are amorphs and produce no detectable products. • lele will not have Lewis antigens, but if Se present will have A, B and H in secretions • Genotype se/se and have one Lewis gene will have Lea in their secretions but no A, B or H. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  10. Lewis Antibodies • Naturally occurring, NOT clinically significant • Almost always IgM • React most often at RT • Agglutination relatively fragile, easily dispersed • May cause ABO discrepancy if reverse cells have Lewis antigen. • Occur almost exclusively in Le (a-b-) and production of anti-Lea AND –Leb not unusual • Anti-Lea frequently encountered, anti-Leb rarely encountered. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  11. Lewis Antibodies • Although most react at RT reactivity may be seen at 37C, but is weaker and may be weakly reactive at AHG • Can bind complement and cause IN-VITRO hemolysis, most often with enzyme treated cells • Antibodies NOTimplicated in HDFN – TWO REASONS • Antibodies are IgM and • Antigens are poorly developed at birth BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  12. I Blood Group (ISBT 027) • Antigens are I or I • Newborns have i antigen • Adults have I antigen • i antigen converts to I as the child matures at about 18 months BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  13. I antibodies • Are IgM, naturally occurring auto-agglutinins with low thermal range. • They are not clinically significant unless they react above 30oC. • Can attach complement (no hemolysis unless it reacts at 37°) • Enzymes can enhance detection BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  14. I antibodies • Anti-I often occurs as anti-IH • This means it will react at different strengths with reagent cells (depending on the amount of H antigen on the RBC) • O cells would have a strong reaction • A cells would have a weaker reaction Remember : strength of H sub. : O > A2 > A2B > B > A1 > A1B. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  15. Anti-I antibodies • Anti-I: • Associated as a cause of Cold Agglutinin Disease • May be secondary to Mycoplasmapneumoniaeinfections • Anti-i: • rare and is sometimes associated with infectious mononucleosis BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  16. P Blood Group (ISBT 003) • Similar to the ABO system • The most common phenotypes are P1 and P2 • P1 – consists of P1 and P antigens • P2 – consists of only P antigens • Like the A2 subgroup, P2 groups can produce anti-P1 • 75% of adults have P1 BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  17. P1 Antigen • Strength of the antigen decreases upon storage • Found in secretions like plasma and hydatid cyst fluid • Cyst of a dog tapeworm BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  18. P antibodies • Anti-P1 • Naturally occurring IgM • Not clinically significant • Can be neutralized by hydatid cyst fluid • Anti-P • Produced in individuals with paroxysmal cold hemoglobinuria (PCH) • PCH – IgG auto-anti-P attaches complement when cold (fingers, toes). As the red cells circulate, they begin to lyse (releasing Hgb) • This PCH antibody is also called the Donath-Landsteiner antibody BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  19. MNSs Blood System • 4 important antigens (more exist): • M • N • S • s • U (ALWAYS present when S & s are inherited) • M & N located on Glycophorin A • S & s and U located on Glycophorin B Remember: Glycophorin is a protein that carries many RBC antigens BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  20. MNSs Antigens M & N only differ in their amino acid sequence at positions 1 and 5 M Glycophorin A N RBC S & s only differ in their amino acid sequence at position 29 S U s Glycophorin B COOH end ….. ….5, 4, 3, 2, 1 (NH2 end)

  21. MNSs antigens • Antigens are destroyed by enzymes (i.e. ficin, papain) • The U antigen is ALWAYS present when S & s are inherited • About 85% of S-s- individuals are U-negative (RARE) • U-negative cells are only found in the Black population BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  22. Frequency of MNSs antigens High-incidence antigen

  23. Thought….. • Can a person have NO MNSs antigens? • Yes, the Mk allele produces no M, N, S, or s antigens • Frequency of 0.00064 or .064% BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  24. Anti-M and anti-N antibodies • IgM (rarely IgG) • Clinically insignificant • If IgG, could be implicated in HDN (RARE) • Will not react with enzyme treated cells BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  25. Anti-S, Anti-s, and Anti-U • Clinically significant • IgG • Can cause RBC destruction and HDN • Anti-U • will react with S+ or s+ red cells • Usually occurs in S-s- cells • Can only give U-negative blood units found in <1% of Black population • Contact rare donor registry BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  26. MNSs Antibody Characteristics BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  27. Systems that Produce Warm-Reacting Antibodies

  28. Kell System • Similar to the Rh system • 2 major antigens (over 20 exist) • K (Kell), <9% of population • k (cellano), >90% of population • The K and k genes are codominant alleles on chromosome 7 that code for the antigens • Well developed at birth • The K antigen is very immunogenic (2nd to the D antigen) in stimulating antibody production BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  29. Kell antigens • Kell antigens have disulfide-bonded regions on the glycoproteins • This makes them sensitive to sulfhydryl reagents: • 2-mercaptoethanol (2-ME) • Dithiothreitol (DTT) • So Kell system Ags are easily inactivated by treating RBCs with these substances. BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  30. Kellnull or K0 • No expression of Kell antigens except a related antigen called Kx • As a result of transfusion, K0 individuals can develop anti-Ku (Ku is on RBCs that have Kell antigens) • Rare Kell negative units should be given BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  31. Kell antibodies • IgG (react well at AHG) • Produced as a result of immune stimulation (transfusion, pregnancy) • Clinically significant • Anti-K is most common because the K antigen is extremely immunogenic • k, Kpb, and Jsb antibodies are rare (many individuals have these antigens and won’t develop an antibody) • The other antibodies are also rare since few donors have the antigen BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  32. Kidd Blood Group • 2 antigens • Jka and Jkb (codominant alleles) BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  33. Kidd Antigens • Well developed at birth • Enhanced by enzymes • Not very accessible on the RBC membrane BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  34. Kidd antibodies • Anti-Jka and Anti-Jkb • IgG • Clinically significant • Implicated in HTR and HDN • Common cause of delayed HTR • Usually appears with other antibodies when detected BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  35. Duffy Blood Group • Predominant genes (codominant alleles): • Fya and Fyb code for antigens that are well developed at birth • Antigens are destroyed by enzymes BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  36. Duffy antibodies • IgG • Do not bind complement • Clinically significant • Stimulated by transfusion or pregnancy (but not a common cause of HDN) • Do not react with enzyme treated RBCs BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  37. The Duffy and Malaria Connection • Most African-Americans are Fy(a-b-) • Interestingly, certain malarial parasites (Plasmodium knowlesi and P. vivax) will not invade Fya and Fyb negative cells • It seems either Fya or Fyb are needed for the merozoite to attach to the red cell • The Fy(a-b-) phenotype is found frequently in West and Central Africans, supporting the theory of selective evolution BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  38. Other Blood Group Antigens…

  39. Lutheran Blood Group System • 2 codominant alleles: Lua and Lub • Weakly expressed on cord blood cells • Most individuals (92%) have the Lub antigen, Lu(a-b+) • The Lu(a-b-) phenotype is RARE BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  40. Lutheran antibodies • Anti-Lua • IgM and IgG • Not clinically significant • Reacts at room temperature • Mild HDN • Naturally occurring or immune stimulated • Anti-Lub • Rare because Lub is high incidence antigen • IgG • Associated with transfusion reactions (rare HDN) BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  41. Cold Antibodies (IgM) • Anti-Lea • Anti-Leb • Anti-I • Anti-P1 • Anti-M • Anti-A, -B, -H • Anti-N LIiPMABHN Naturally Occurring BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  42. Warm antibodies (IgG) • Rh • Kell • Duffy • Kidd • S,s • U BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  43. Remember enzyme activity: Papain, bromelin, ficin, and trypsin BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

  44. Thanks BB. MLT309. 2013-2014.Lec.6.Mr. Waggas

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