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Handouts Program-Handouts.Aspx Handouts http://www.immucor.com/en-us/Pages/Educational- Program-Handouts.aspx 2 All Content © Immucor, Inc. 2019 Advanced Track Webinars Link to register: https://immucor.webinato.com/register 3 All Content © Immucor, Inc. 2019 Advanced Track Webinars Link to register: https://immucor.webinato.com/register 4 All Content © Immucor, Inc. 5 All Content © Immucor, Inc. Link to register: https://immucor.webinato.com/register 6 All Content © Immucor, Inc. learn.immucor.com 7 All Content © Immucor, Inc. Continuing Education • PACE, Florida and California DHS • 1.0 Contact Hours • Each attendee must register to receive CE at: https://www.surveymonkey.com/r/TheJollyBloodBanker • Registration deadline is April 5, 2019 • Certificates will be sent via email only to those who have registered April 19, 2019 8 All Content © Immucor, Inc. Questions? • You are all muted • Q&A following session - Type in questions 9 All Content © Immucor, Inc. • Course content is for information and illustration purposes only. Immucor makes no representation or warranties about the accuracy or reliability of the information presented, and this information is not to be used for clinical or maintenance evaluations. • The opinions contained in this presentation are those of the presenter and do not necessarily reflect those of Immucor. 10 All Content © Immucor, Inc. The Jolly Blood Banker and “Other” Blood Groups Jill R. Storry, PhD FIBMS Associate Professor, Lund University Technical Director, Immunohematology Clinical Immunology and Transfusion Medicine, Lund Blood systems covered in this talk: • MNS • Kell • Lewis • Duffy • Kidd 36 blood group systems are carried on functional molecules Host defence/innate immunity ABO P1PK Enzymes Lewis FORS GLOB H (Glyco)proteins of I structural or unknown function LW Xg Transporters Duffy and channels Lutheran Indian Scianna Raph Complement JMH regulation Oka Adhesion molecules The MNS Blood Group System (ISBT 002) • MNS antigens are carried on: GPA GPB Hybrids of GPA & GPB • Specific to red blood cells • Highly polymorphic system – 49 antigens • Function of GPA and GPB not completely understood: Chaperone proteins? Protection by sialic acid? Antigens of the MNS blood group system Prevalence n Antigens Variable 4 M N S s High 10 Ena ENKT ENEP ENEH ENAV U ‘N’ ENDA ENEV JENU Low 35 He Mia Mc Vw Mur Mg Vr Me Mta Sta Ria Cla Nya Hut Hil Mv Far sD Mit Dantu Hop Nob Or DANE TSEN MINY MUT SAT ERIK Osa HAG MARS MNTD SARA KIPP MNS antigens are carried on GPA and GPB 20 M/N 20 ’N’ Trypsin sites α-chymotrypsin at aa 50 & 58 site at aa 51 Papain site Papain site ~aa 54 at aa 78/80 48 S/s RBC lipid bilayer 91 Numbering: 150 Counted from initiating N-linked sugar Methionine (19aa leader O-linked sugar sequence included) The GYPA gene family Chromosome 4q31.21 GYPA GYPB GYPE GYPA 1 2 3 4 5 6 7 GYPB 1 2 3 4 5 6 GYPE 1 2 3 4 5 6 High nucleotide identity Low nucleotide identity Molecular Basis of MNS Antigens Mechanisms for generating diversity: • Single nucleotide polymorphisms (SNPs) • Deletions/insertions • Gene recombination events All of the above are reported for the MNS system MNS SNPs Single nucleotide polymorphisms are an effective method of creating diversity, e.g. S/s antigens GYPB exon 4 GA GAA ATG GGA CAA CTT GTC CAT CGT TTC ACT GTA CCA G S E M G Q L V H R F T V P GA GAA ACG GGA CAA CTT GTC CAT CGT TTC ACT GTA CCA G s E T G Q L V H R F T V P SNPs Encode Low Incidence Antigens 20 M/N 23 Mg 24 36 MNTD 46 Nya 20 47 Vw/Hut 22 MV ‘N’ 24 50 Or 66 Vr 73 Osa 76 Ria 48 S/s 77 Mta SARA 80 78 ERIK 54 Mit 82 MARS 84 HAG 58 sD Numbering: 91 GPB Counted from initiating GPA Methionine (19aa 150 sequence included Homology Between Genes Creates Diversity GYPA 1 2 3 4 5 6 7 t GYPB 1 2 3 4 5 6 High nucleotide identity Low nucleotide identity Recombination hotspot Creation of MNS hybrid genes Unequal crossover GP.Sch GYPB GYPA GYPB GYPA St(a+) Novel antigens are GP.Hil (MINY+, Hil+) created at GYPA GYPB GP.JL (MINY+, TSEN+) crossover points GP.TK (SAT+) Gene conversion New antigens are encoded by GYPA GYPB -A -B the novel hybrid sequence DNA exchange by double GYPA GYPB strand break repair (DSBR) mechanism leaves one chromosome unaltered Different mechanisms can produce the same antigen GP.Hil G GP.Mur P Generated by G P Generated by E unequal crossover P B E gene conversion A E T A Hil G Hil E G T G P G P B D B L GP.Hil GPMur GP.Bun GP.HF MNS Antigens Produced by Hybrids • Mia, Hut, Mur, MUT, Hil, TSEN, MINY, Hop, Nob, DANE, Sta, Dantu, SAT • Antibodies can cause HDN • The GP.Mur (Mi.III) phenotype is ~15% in Chinese populations • HDN due to ”anti-Mia” is a concern • Anti-Mur +/- MUT • One of the most common antibodies in Asian populations High Prevalence MNS antigens 20 EnaFS 20 47 ENEH/Vw/Hut ‘N’ 24 Ena 68&71 ENKT 48 EnaFR 81 ENEV 82 ENAV/MARS U 84 ENEP/HAG 59 GPA 91 GPB 150 ENDA: encoded by GYPA absent from JENU: encoded by GYPB, absent from GP.Dane hybrid GP.Mur hybrid Null Phenotypes in the MNS System • En(a−): absence or alteration of GPA • S−s− : absence or alteration of GPB • MkMk phenotype: absence of GPA and GPB Clinical significance of MNS antibodies Anti- Ig class HTR HFDN Comments M IgM/IgG Rarely Rarely Worth monitoring in pregnancy N IgM>IgG No No S IgG Yes Yes s IgG Rarely Rarely U IgG Yes Yes Ena IgG Rarely Rarely Can be an autoantibody ’N’ IgG Yes Yes ’Lows’ IgM>IgG No Yes Mabye naturally occurring Many low prevalence MNS antigens have been detected as a consequence of HDFN in women with negative antibody screens. Disease can range from mild to severe. The Kell Blood Group System (ISBT 006) • 1st antibody – anti-K, identified in 1946 in a report of HDFN • 36 antigens • Kell is expressed on: • RBCs, erythropoietic tissues, testes • Lower expression in brain, lymphoid organs, muscle (heart and skeletal) Kell blood group system antigens 001 002 003 004 005 006 K k Kpa Kpb Ku Jsa 007 008 009 010 011 012 Jsb --- --- Ula K11 K12 013 014 015 016 017 018 K13 K14 --- K16 K17 K18 019 020 021 022 023 024 K19 Km Kpc K22 K23 K24 025 026 027 028 029 030 VLAN TOU RAZ VONG KALT KITM 031 032 033 034 035 036 KYO KUCI KANT KASH KELP KETI 037 038 039 KHUL KYOR KEAL Low High Geographic variation in expression of low prevalence antigens Antigen Ethnic group Occurrence Others K Whites 9% <2% Arabs 25% Jsa Blacks (USA) 20% <0.01% Ula Finns 2.6% <0.01% Kpc Japanese 0.32% <0.01% The KEL gene is located on chromosome 7 Chromosome 7q33 - KEL 19 exons 21,5 kb introns exons ..ccccctctctctcctttaaag Exons contain coding nucleotides CTT GGA GGC TGG CGC ATC TCT GGTIntrons AAA containTGG ACT non TCC-coding TTA nucleotides: AAC TTT AAC CGA ACG CTG AGA. HighCTT percentageCTG ATG AGT of theCAG gene TAT is GGCnoncoding CAT TTC but itCCT TTC TTC AGAcontains GCC TACimportant CTA GGA regulatory CCT CAT sequences CCT GCC TCT CCA CAC ACA CCA GTC ATC CAG gtgagggatg...... The Kell glycoprotein • Type 2 membrane protein 732aa; Mr 93 kDa 15 cysteine residues: predicts a heavily folded protein Glycosylated 5 (4) N-linked branched oligosaccharides • One of M13 family of neutral zinc endopeptidases • Specifically cleaves big endothelin-3 to ET-3 ET-3 is a powerful vasoconstrictor • Biological role on RBCs is still unknown Kell antigens are created by missense SNPs K23–/K23+ 1145A>G TOU+/TOU– 1217G>A K13+/K13– 986T>C KUCI+/KUCI– 1271C>T K22+/K22– 965C>T KANT+/KANT– 1283G>T KETI+/KETI– 1391C>T KTIM+/KYIM– 913G>A K19+/K19– 1475G>A 11 12 K11/K17 905T/C 10 13 Ul(a–)/Ul(a+) 1481A>T KHUL/KEAL 877C>T KYOR/KYO 875G/A 9 14 Kpb/Kpc 842G/A Kpa/Kpb 841T/C 8 15 K12+/K12– 1523A>G KELP+/KELP– 780G>T KASH+/KASH– 758A>G 7 16 RAZ+/RAZ– 745G>A VLAN–/VLAN+ 743G>A 17 Jsa/Jsb 1790C/T VONG–/VONG+ 742C>T 6 KELP+/KELP– 2024G>A K/k 578T/C 5 18 K14/K24 538G/C KALT+/KALT– 1868G>A 4 19 K18+/K18– 388C>T; 389G>A 3 Reid, Lomas-Francis & Olsson The blood group antigen factsbook, 3rd ed. 2 Slide modified from ES Wester et al. Transfusion 2005,45:545 1 KEL Kell glycoprotein interacts with XK 11 12 10 13 9 14 15 8 15 16 7 H Exons 1-19 Kell E 6 L 17 L H 5 18 4 COOH 19 3 XK 2 1 NH2 KEL N-glycans Cys347=Cys72 Preferential processing of big ET-3 by wild-type s-Kell Lee S et al. Blood 1999;94:1440-1450 S-Kell: His-tagged extracellular domain of Kell gp ©1999 by American Society of Hematology The K0 phenotype • Null phenotype of the Kell system All Kell antigens are absent Expression of Kx is elevated Amount of XK protein is reduced • No apparent physiological defect • Reported in all populations • May produce anti-Ku (KEL5) • Many molecular backgrounds Missense mutations Nonsense mutations Altered splicing due to intron mutations Preferential processing of big ET-3 by RBCs of common Kell phenotype: comparison with K0 phenotype Lee S et al.
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