DOCSLIB.ORG

ISBT Working Party on Terminology for Red Cell Surface Antigens J

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
ISBT Working Party on Terminology for Red Cell Surface Antigens J International Society of Blood Transfusion Societe lnternationale de Transfusion Sanguine Section Editor: H. Gunson, Manchester Vox Sang 1995;69:265-279 G. L. Daniels (Chair) D. J. Anstee, J. I? Cartron Blood Group Terminology 1995 ctl Dahr; I?D. Issitt ISBT Working Party on Terminology for Red Cell Surface Antigens J. J~irgensen,L. Kornstad C. Levene, C. Lomas-Francis A. Lubenko, D. Mallory J.J. Moulds, t: Okubo M. Overbreke, M. E. Reid I? Rouger, S. Seidl I? Sistonen, S. Wendel G. Woodfield, i? Zelinski Since the first human blood groups were discovered al- tions on red cell antigens. Much of the information provided most a century ago, many hundreds of new red cell antigens in the 1990 monograph [l] is reiterated here so that referral have been identified. Because of the extended time period back will not generally be required, but only references after over which these antigens were discovered, a variety of dif- 1990 are provided. ferent terminologies has been introduced. In some cases single capital letters were used (A, B, M, K), in some super- scripts distinguished allelic products (Fy’, Fyh),and in some ISBT Numerical Terminology a numerical notation was introduced (Fy3). Some antigens were given different names in different laboratories, based The mandate of the Working Party is to provide a termi- on alternative genetic theories (D and Rho). nology for red cell surface antigens. By definition, these an- In 1980 the International Society of Blood Transfusion tigens must be defined serologically by the use of a specific (ISBT) established a Working Party to devise a genetically antibody. Numerical designations and blood group symbols based numerical terminology for red cell surface antigens. cannot be allocated to nucleotide or amino acid sequences, In 1990 the Working Party published a monograph describ- or to restriction fragment length or other DNA polymor- ing a numerical terminology for 242 red cell antigens [I], phisms, even though the presence of specific blood group and brief updatings followed in 1991 [2] and 1993 [3]. In the antigens may be signposted by these techniques. All anti- 6 years since the 1990 report many amendments to the clas- gens receiving ISBT numbers must have been shown to be sification have been necessary: 18 new antigens have been inherited characters. identified and 6 others declared obsolete due to lack of suit- All authenticated antigens fall into one of 4 classifica- able reagents; four new systems have been created (all from tions: systems; collections; low incidence antigens (700 se- existing collections); the Auberger antigens joined the ries), and high incidence antigens (901 series). A blood Lutheran system; the Gregory antigens and Jo” joined the group system consists of 1 or more antigens controlled at a Dombrock system; the Wright antigens joined the Diego single gene locus, or by 2 or more very closely linked ho- system. Furthermore, since, 1990, many of the blood group mologous genes with little or no observable recombination genes have been isolated: of the genes controlling the 23 between them. Each system has been shown to be genetical- systems, only four (PI, JK, SC, DO) remain to be cloned. ly discrete from every other system. Collections consist of The purpose of this monograph is to describe the ISBT serologically, biochemically, or genetically related antigens terminology for red cell surface antigens and to tabulate the which do not fit the criteria required for system status. The complete 1995 version of the classification. In addition, an 700 and 901 series contain low and high incidence antigens, alternative ‘popular’ terminology is suggested in an attempt respectively, which cannot be included in a system or col- to reduce the number of different names used in publica- lection. Dr. G. L. Daniels 0 1995 S.Karger A(;, Uasel Bristol institute for Transfusion Sctence 0042 ‘3007195/06~)3-0265 Southmead Road R 8 OO!O Bristol BSiO 5ND (UK) Each antigen belonging to a blood group system is iden- designated by the system symbol, followed by a space (or tified by a 6-digit number (table 1-3). The first 3 digits rep- asterisk), followed by the antigen number (e.g. KEL 3). Gc- resent the system (e.g. 006 for Kell), and the second 3 the notypes have the system symbol, followed by a space (or specificity (e.g. 006003 for Kp"). Alternatively, the system asterisk), followed by alleles or haplotypes separated by a symbol followed by the antigen number may be used (e.g. slash (e.g. KEL 2,3/2,4). Amorph or null genes are repre- KEL003 or, more usually, KEL3 as sinistral zeros may be sented by a 0 (e.g. KEL 2,3/0). Gene and genotype desig- removed). Phenotypes are represented by the system sym- nations are italicized (or underlined). Antigen, phenotype, bol, followed by a colon, followed by a list of antigens sep- gene, and genotype designations for collections are con- arated by commas. Those antigens shown to be absent are structed in the same way. For the 700 and 901 series, 700 or preceded by a minus sign (e.g. KEL:-1,2,-3,4). Genes are 901 replaces the system symbol. Symbols for Gene Loci Table 1. Examples of antigen, phenotype, gene, and genotype des- ignations in the traditional and ISBT terminologies The symbol for a gene or cluster of genes controlling a Traditional ' ISBT blood group system is the italicized symbol for the system (e.g. CO for the gene controlling the Colton system). How- Antigen Lu" 005001 or LUI ever, the genes controlling most of the blood group systems Phenotype Lu(a-b+) LU:-I, 2 Gene Lu" LU I have been cloned and in many cases the gene locus has an Lu LUO alternative symbol (table 2), usually because the protein Gcnotypc Lu" L~lii L u 2/2 product of the gene is of known function or the gene had an Lu" Lu'/Lu'' LdJ LU 1.8/2,14 existing symbol before the association with the blood group la'' LllC'/LU L u 2,K/O was known. Examples: the gene controlling expression of ' And 'popular' alternative the Diego antigens is the anion exchanger 1 gene AEI [25, 261; the Yt antigens are encoded by the acetylcholinesterase Table 2. Thc blood group systems, the genes that encode them, and their chromoso- No. System name System Gene name(s) Chromosomal References iiial location symbol location 00 1 ABO ABO ABO 9q34.1Lq34.2 4 002 MNS MNS GYPA, GYPB, GYPE 4q28-q3 1 1 003 P PI PI 22q 1 1.2-qter 1 004 Rh RH RHD, RHCE lp36.2-~34 5-8 005 Lutheran LU LU 19q12-q 13 9 006 Kell KEL KEL 7q33 10-12 007 Lewis LE FUT3 19~13.3 13-1 7 008 Duffy FY FY 1 q22-q23 18- 22 009 Kidd JK .JK 18ql I-qI2 23 010 Diego DI AEI 17q 12-q2 1 24-26 01 1 Yt YT ACHE 7q22 27-29 012 xg XG XG Xp22.32 30,3 1 013 Scianna SC sc 1 p36.2Lp22.1 1 014 Dombrock DO DO Not known 015 Colton CO AQPl 7p14 32,33 016 Landsteiner-Wiener LW LW 19~13.2-cen 34 017 ChidoIRodgers CHIRG C4A, C4B 6p2 1.3 I 018 Hh H FUTI 19q13 35,36 019 Kx XK XK xp21.1 37 020 Gerbich GE GYPC 2q 14-q2 1 I 02 1 Cromer CROM DAF 1 q32 I 022 Knops KN CR1 1 q32 38.39 023 Indian IN CD44 I lp13 I 266 ISBT Working Party Blood Group Terminology 1995 Table 3. Antigens of the blood group systems System Antigen number 001 002 003 004 005 006 007 008 009 010 011 012 013 014 015 016 017 001 ABO A B A,B A1 ... ~~ 002 MNS M N S s U He Mi" M' Vw Mur Mg Vr Me Mt" Sta RI" Cla ~~~ ~~- ~.003 P ~.P1 ... ... 004 RH---. DCEc e_ f Ce C" Cx V E" G ... ... ... ... Hr,, 005 LU __ LU~ Luh Lu3 Lu4 Lu5 Lu6 Lu7 Lu8 Lu9 ... Lull Lu12 Lu13 Lu14 ... Lu16 Lu17 006 KEL K k Kp" Kph Ku Js" Jsh ... ... UI8 K11 K12 K13 K14 ... K16 K17 ~-007 LE .__Lea Leh Leah ___~_008 FY Fy" Fyh Fy3 Fy4 Fy5 Fy6 009 JK Jk" Jkh Jk3 010 DI Did Dih Wr" Wrh ~~~~ 011 YT Yt" Yth ~___ 015 CO _ cod Coh Co3 016 LW ... ... ... .. Lwa LW'b LWh ~~ 017 CH/RG Chl Ch2 Ch3 Ch4 Ch5 Ch6 WH Rgl Rg2 rH- H ~-0TXK~ Kx 020 GE .. Ge2 Ge3 Ge4 Wb Ls" Ana Dh" ~-TCROM Cf Tcd Tch Tc' Drd Esa IFC WESa WESh UMC 022 KN- _____Kn" Knh McC" SId Yk" 023 IN- Ina Inh System Antigen number 018 019 020 021 022 023 024 025 026 027 028 029 030 031 032 033 034 002 MNS Ny" Hut Hi1 M"~- Far sD Mit Dantu Hop Nob En" En'KT 'N' Or DANE TSEN MINY ~-004~~- Hr hr' VS C" CF D" . c-like cE hrH Rh29 Go" hrB Rh32 Rh33 HrB ~-005 LU-- Au' Aub Lu20 006 KEL K18 K19 Km Kp' K22 K23 K24 System Antigen number 035 036 037 038 039 040 041 042 043 044 045 046 047 048 049 50 051 002 MNS __ MUT SAT ERIK 0s" 004 RH- Rh35 Be" Evans ... Rh39 Tar Rh41 Rh42 Craw- Nou RIV Sec Dav JAL STEM FPTT MAR ford . = Obsolete (table 7). 267 gene ACIfE [28, 291; the Colton antigens are encoded by Modifications since 1990: Existing Systems AQf 1, the gene producing a water transporter Aquaporin 1 002, The MNS System.
Load more

Recommended publications
  • Other Blood Group Systems—Diego,Yt, Xg, Scianna, Dombrock
    Review: other blood group systems—Diego, Yt, Xg, Scianna, Dombrock, Colton, Landsteiner- Wiener, and Indian K.M. B YRNE AND P.C. B YRNE Introduction Diego Blood Group System This review was prepared to provide a basic The Diego blood group system (ISBT: DI/010) has overview of “Other Blood Groups.” Some of the more expanded from its humble beginnings to now include major blood group systems, i.e., ABO, Rh, Kell, Duffy, up to 21 discrete antigens (Table 1). 3 Band 3, an anion and Kidd, are also reviewed in this issue and are not exchange, multi-pass membrane glycoprotein, is the covered here. The sheer mass of data on the MNS basic structure that carries the Diego system antigenic blood group system is so extensive and complicated determinants. 4 The gene that encodes the Band 3 that it justifies a review all of its own, and it is therefore protein is named SLC4A1 and its chromosomal location not discussed in this article. However, various aspects is 17q12–q21. 4 of MNS were described in recent papers in Di a and Di b are antithetical, resulting from a single Immunohematology. 1,2 nucleotide substitution (2561T>C) that gives rise to The blood group systems that are covered are those amino acid changes in the Band 3 protein (Leu854Pro). that most workers believe to have some degree of To date, the Di(a–b–) phenotype has not been clinical importance or interesting features: Diego (DI), described. The Di a and Di b antigens are resistant to Yt (YT), Xg (XG), Scianna (SC), Dombrock (DO), Colton treatment with the following enzymes/chemicals: (CO), Landsteiner-Wiener (LW), and Indian (IN).
    [Show full text]
  • Blood Bank I D
    The Osler Institute Blood Bank I D. Joe Chaffin, MD Bonfils Blood Center, Denver, CO The Fun Just Never Ends… A. Blood Bank I • Blood Groups B. Blood Bank II • Blood Donation and Autologous Blood • Pretransfusion Testing C. Blood Bank III • Component Therapy D. Blood Bank IV • Transfusion Complications * Noninfectious (Transfusion Reactions) * Infectious (Transfusion-transmitted Diseases) E. Blood Bank V (not discussed today but available at www.bbguy.org) • Hematopoietic Progenitor Cell Transplantation F. Blood Bank Practical • Management of specific clinical situations • Calculations, Antibody ID and no-pressure sample questions Blood Bank I Blood Groups I. Basic Antigen-Antibody Testing A. Basic Red Cell-Antibody Interactions 1. Agglutination a. Clumping of red cells due to antibody coating b. Main reaction we look for in Blood Banking c. Two stages: 1) Coating of cells (“sensitization”) a) Affected by antibody specificity, electrostatic RBC charge, temperature, amounts of antigen and antibody b) Low Ionic Strength Saline (LISS) decreases repulsive charges between RBCs; tends to enhance cold antibodies and autoantibodies c) Polyethylene glycol (PEG) excludes H2O, tends to enhance warm antibodies and autoantibodies. 2) Formation of bridges a) Lattice structure formed by antibodies and RBCs b) IgG isn’t good at this; one antibody arm must attach to one cell and other arm to the other cell. c) IgM is better because of its pentameric structure. P}Chaffin (12/28/11) Blood Bank I page 1 Pathology Review Course 2. Hemolysis a. Direct lysis of a red cell due to antibody coating b. Uncommon, but equal to agglutination. 1) Requires complement fixation 2) IgM antibodies do this better than IgG.
    [Show full text]
  • Genetic Variants Within the Erythroid Transcription Factor, KLF1, And
    Accepted Manuscript Genetic Variants within the Erythroid Transcription Factor, KLF1, and Reduction of the Expression of Lutheran and Other Blood Group Antigens: Review of the in(Lu) Phenotype Nicole S. Fraser, Christine M. Knauth, Assia Moussa, Melinda M. Dean, Catherine A. Hyland, Andrew C. Perkins, Robert L. Flower, Elizna M. Schoeman PII: S0887-7963(18)30146-9 DOI: https://doi.org/10.1016/j.tmrv.2019.01.004 Reference: YTMRV 50565 To appear in: Transfusion Medicine Reviews Please cite this article as: N.S. Fraser, C.M. Knauth, A. Moussa, et al., Genetic Variants within the Erythroid Transcription Factor, KLF1, and Reduction of the Expression of Lutheran and Other Blood Group Antigens: Review of the in(Lu) Phenotype, Transfusion Medicine Reviews, https://doi.org/10.1016/j.tmrv.2019.01.004 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT Genetic variants within the erythroid transcription factor, KLF1, and reduction of the expression of Lutheran and other blood group antigens: review of the In(Lu) phenotype Nicole S. Fraser* a,b, Christine M. Knauth* a,b , Assia Moussa a,b, Melinda M. Dean a, Catherine A. Hyland a,b, Andrew C.
    [Show full text]
  • Jka, Jkb, Jk – Co-Dominant Inheritance – Jk Is a Silent Allele
    Kidd Blood Group System Qun Lu, MD Assistant Professor Division of Transfusion Medicine Department of Pathology and Laboratory Medicine UCLA, School of Medicine Los Angeles, California 02-05-2009 History of Kidd Blood Group System . Jka was discovered in 1951 by Allen: Mrs. Kidd had hemolytic disease of newborn (HDN) in her son. A new RBC alloantibody was detected in her serum, reacted with her husband’s RBCs. Jkb was found in 1953 by Plaut . The antigens were independent of other known blood groups. They named after Mrs. Kidd. Jk null phenotyp was found in 1959 by Pinkerton. Since the specificities were inseparable, the antibody was renamed anti-Jk3 which recognizes an antigen found whenever Jka or Jkb is present. ISBT Human Blood Group Systems ISBT Number Name Abbreviation 001 ABO ABO 002 MNS MNS 003 P P 004 Rh RH 005 Lutheran LU 006 Kell KEL 007 Lewis LE 008 Duffy FY 009 Kidd JK 010 Diego DI 011 Cartwright YT 012 XG XG 013 Scianna SC 014 Dombrock DO 015 Colton CO 016 Landsteiner-Wiener LW 017 Chido/Rodgers CH/RG 018 Hh H 019 Kx XK 020 Gerbich GE 021 Cromer CROM 022 Knops KN 023 Indian IN 024 Ok OK 025 Raph RAPH Kidd Antigens . Genotype: – Genes located on chromosome 18 – Three alleles Jka, Jkb, Jk – Co-dominant Inheritance – Jk is a silent allele . Common antigen ---- JK3 Ag: – Present with Jka and/or Jkb antigens – Whenever you have Jka or Jkb antigens on the RBC you also have Jk3 antigen. – Anti- Jk3 is against Jka,Jkb, Jk3 antigens, transfuse with Jk(a-b-) blood, very difficult to find Homozygous Heterozygous for Jka or Jkb for JKa and Jkb.
    [Show full text]
  • An Introduction to Blood Groups
    1405153490_4_001.qxd 8/16/06 9:21 AM Page 1 An introduction to blood groups CHAPTER 1 What is a blood group? In 1900, Landsteiner showed that people could be divided into three groups (now called A, B, and O) on the basis of whether their red cells clumped when mixed with separated sera from people. A fourth group (AB) was soon found. This is the origin of the term ‘blood group’. A blood group could be defined as, ‘An inherited character of the red cell surface, detected by a specific alloantibody’. Do blood groups have to be present on red cells? This is the usual meaning, though platelet- and neutrophil-specific antigens might also be called blood groups. In this book only red cell surface antigens are considered. Blood groups do not have to be red cell specific, or even blood cell specific, and most are also detected on other cell types. Blood groups do have to be detected by a specific antibody: polymorphisms suspected of being present on the red cell surface, but only detected by other means, such as DNA sequencing, are not blood groups. Furthermore, the antibodies must be alloantibod- ies, implying that some individuals lack the blood group. Blood group antigens may be: • proteins; • glycoproteins, with the antibody recognising primarily the polypeptide backbone; • glycoproteins, with the antibody recognising the carbohydrate moiety; • glycolipids, with the antibody recognising the carbohydrate portion. Blood group polymorphisms may be as fundamental as representing the presence or absence of the whole macromolecule (e.g. RhD), or as minor as a single amino acid change (e.g.
    [Show full text]
  • The Kidd System
    A review: the Kidd system R. MOUGEY After the rediscovery of the principle of the an- The antibody is not thought to be merely anti-Jk sup(a) + tiglobulin test and its introduction as the direct or in- anti-Jksup(b), because immunized Jk(a- b - ) individuals make direct "Coombs" test, there was a period of rapid anti-Jk3 whether they are sensitized by the Jksup(a) or Jk sup(b) discovery of new blood group systems that were im- antigen. Also the sera of Jk(a-b-) individuals often portant to blood transfusion therapy. One of the most contain a separable anti-Jksup(a) or -Jksup(b) component. Since important was the recognition of the Kidd blood group no individual has yet been found that is Jk(a+) or Jk(b+) system in 1951.sup(1) The patient, a Mrs. Kidd, had a new and Jk: - 3, the anti-Jk3 is thought to recognize a shared antibody in her serum and gave birth to an infant with determinant that is on all red cells of common Jk hemolytic disease of the newborn (HDN). The antibody phenotypes. The most recent evidence in support of was named anti-Jksup(a) The "J" was added to avoid con- the Jk3 antigen is the discovery of persons who are fusion with the Kell antigen. In retrospect, this case phenotypically Jk(a -b - ), Jk:3.5 of HDN is a curiosity since Kidd antibodies do not There is some controversy about the expression of typically cause significant HDN.sup(2) Other examples were theJk3 antigen in the presence of the Jk gene.
    [Show full text]
  • Essentials of Blood Group Antigens and Antibodies
    Essentials of Blood Group Antigens and Antibodies Non-Medical Authorisation of blood Components Nov 2017 East Midlands Regional Transfusion Committee Transfusion Terminology Antigens and Antibodies Antibodies Antigens Blood Group Antigens • Antigens are part of the surface of cells – Red Cells have “Blood group antigens” – White cells and platelets have HLA antigens (platelets also have HPA antigens) https://www.ncbi.nlm.nih.gov/books/NBK2264/bin/imagemap.jpg Reactions to blood usually occurs when the antigen on the donor cells reacts with an antibody in the patient’s plasma What Are Blood Group Antigens? • Complex structures that contain protein and carbohydrate • Part of the membrane structure – blood group antigens often have a role e.g. structural, transport • Produced by inheritance of specific genes – genes produce different antigen options within one blood group system http://en.wikibooks.org/wiki/Structural_Biochemistry/Lipids/Lipid_Bilayer Blood Group Antigens • Currently 36 known blood group systems • Most clinically important are ABO and Rh • Antigens on donor red cells can stimulate a patient to produce an antibody, if the patient lacks the antigen themselves • Likelihood of antibody production is low but increases the more transfusions that are given What are Blood Group Antibodies? • Protein molecules - called https://en.wikipedia.org/wiki/Antibody#/medi a/File:Antibody.svg immunoglobulins (Ig) • Found in the plasma/serum – Produced by the immune system following exposure to a foreign antigen – Antibodies bind specifically
    [Show full text]
  • Disorders of the Red Cell Membrane
    IRON2009_CAP.16(402-435):EBMT2008 4-12-2009 16:32 Pagina 402 * CHAPTER 16 Disorders of the red cell membrane Jean Delaunay, Jean-Pierre Cartron IRON2009_CAP.16(402-435):EBMT2008 4-12-2009 16:32 Pagina 403 CHAPTER 16 • Disorders of the red cell membrane 1. Introduction The red cell membrane designates, in a strict sense, the plasma membrane of the erythrocyte, the only membrane remaining in the circulating red cell. It consists of a lipid bilayer, a variety of proteins studded therein, and the glycans that stick outward, being linked covalently either to proteins or to lipids. Protein or glycan domains constitute the structural bases of blood groups. In a wider sense, the red cell membrane includes, in addition, an unusually thick, bidimensional protein network that provides the red cell with its mechanical properties of both resistance and flexibility. This protein network is named the red cell skeleton. Most of the genes encoding the membrane proteins are known. Mutations in these genes account for a variety of different conditions, most of which are haemolytic anaemias of various descriptions. 2. The red cell membrane A schematic picture of the red cell membrane is shown in Figure 1. A classical description of the lipid bilayer was provided in a review by Lux and Palek (1). During the last decade, a major breakthrough has been the discovery of lipid rafts in membranes in general, and in the red cell membrane in particular. Rafts are detergent-resistant plasma membrane microdomains. They are rich in sphingolipids. They are also rich in cholesterol. They exist as islets having a phase different to that of the loosely packed disordered state of the rest of the bilayer.
    [Show full text]
  • SPECIFICATION SPN214/4 the Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion Copy Numb
    SPECIFICATION SPN214/4 The Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion This Specification replaces Copy Number SPN214/3 Effective 03/05/17 Summary of Significant Changes Change of author to Nicole Thornton from Geoff Daniels (retired). Update to blood group systems (new systems added) Update to some rare antibodies due to availability of new data Change of regional coordinators and associated contact information Removal of unnecessary information to improve clarity Purpose This document outlines current knowledge on the clinical significance of blood group alloantibodies. Its prime purpose is to enable clinical decisions to be made regarding the management and blood transfusion support of patients with blood group antibodies that are not commonly encountered and for which antigen-negative blood is not available in the routine stock. The overall aim is to ensure that a uniform RCI Clinical Policy for the supply of blood for transfusion is implemented throughout the NHSBT. Definitions BSH British Committee for Standards in IAT Indirect Antiglobulin Test Haematology IBGRL International Blood Group DHTR Delayed Haemolytic Transfusion Reference Laboratory Reaction IRDP International Rare Donor Panel HDFN Haemolytic Disease of the Fetus NHSBT NHS Blood and Transplant and Newborn NFBB National Frozen Blood Bank HTR Haemolytic Transfusion Reaction RCI Red Cell Immunohaematology Applicable Documents ESD121 Guidelines for pre-transfusion INF1302: HGP project – targets, phenotype compatibility procedures
    [Show full text]
  • Red Blood Cell Molecular Testing AHS-M2170
    Corporate Medical Policy Red Blood Cell Molecular Testing AHS-M2170 File Name: red_blood_cell_molecular_testing Origination: 7/2020 Last CAP Review: 8/2021 Next CAP Review: 8/2022 Last Review: 8/2021 Description of Procedure or Service The first successful blood transfusion can be dated back to the 1600s (Osterman & Arora, 2017), and molecular testing methods to analyze blood samples were introduced to the transfusion medicine community in the 1990s (Westhoff, 2006). Several ailments may warrant a blood transfusion, and the phenotypic and genotypic determination of red blood cell antigens assist in limiting immune responses in transfusion patients. Agglutination tests via serology have been the gold standard for determining blood group antigens for more than 100 years (Boccoz, Le Goff, Blum, & Marquette, 2015), yet newer molecular techniques may grant added specificity (Elite, 2015a). Related Policies: Prenatal Screening AHS-G2035 Genetic Testing for Alpha- and Beta Thalassemia AHS-M2131 ***Note: This Medical Policy is complex and technical. For questions concerning the technical language and/or specific clinical indications for its use, please consult your physician. Policy BCBSNC will provide coverage for red blood cell molecular testing when it is determined to be medically necessary because the medical criteria and guidelines shown below are met. Benefits Application This medical policy relates only to the services or supplies described herein. Please refer to the Member's Benefit Booklet for availability of benefits. Member's benefits may vary according to benefit design; therefore member benefit language should be reviewed before applying the terms of this medical policy. When Red Blood Cell Molecular testing is covered Red cell genotyping (including C, c, D, E, e, K, k, Jka, Jkb, Fya, Fyb, S, s,U) is considered medically necessary for the following: a.
    [Show full text]
  • Clinical Significance of Antibodies to Antigens in the Scianna
    R EVIEW Proceedings from the International Society of Blood Transfusion Working Party on Immunohaematology, Workshop on the Clinical Significance of Red Blood Cell Alloantibodies, September 2, 2016, Dubai Clinical significance of antibodies to antigens in the Scianna, Dombrock, Colton, Landsteiner- Weiner, Chido/Rodgers, H, Kx, Cromer, Gerbich, Knops, Indian, and Ok blood group systems S. Lejon Crottet This article reviews information regarding the clinical Table 1. Antigen and antibody characteristics of the Scianna significance of antibodies to antigens in the Scianna, Dombrock, blood group system Colton, Landsteiner-Wiener, Chido/Rodgers, H, Kx, Cromer, Antigen Antibody Gerbich, Knops, Indian, and Ok blood group systems. Like most blood group systems, antibodies to many of the antigens in these ISBT name Trivial name Prevalence HTR HDFN groups are rarely encountered because of the high prevalence SC1 Sc1 High No report No report (DAT+) of the associated antigens in most populations. For many, the SC2 Sc2 Low No No to Mild clinical significance—that is, the potential to cause reduced (1 case) (DAT+) survival of transfused antigen-positive red blood cells or a SC3 Sc3 High No to mild/ Mild transfusion reaction (e.g., anti-Ge2, anti-H) and/or hemolytic delayed disease of the fetus and newborn (e.g., anti-Coa, anti-Ge3)— has been documented. Some of these antibodies are not always SC4 Rd Low No Mild to severe clinically significant, and because of the high prevalence of the SC5 STAR High No report No report antigen, antigen-negative blood may be extremely difficult to find SC6 SCER High No report No report (e.g., anti-LW, anti-Inb).
    [Show full text]
  • Do Blood Group Antigens and the Red Cell Membrane Influence Human
    cells Review Do Blood Group Antigens and the Red Cell Membrane Influence Human Immunodeficiency Virus Infection? Glenda M. Davison 1,2,* , Heather L. Hendrickse 1 and Tandi E. Matsha 1 1 SAMRC/CPUT/Cardiometabolic Health Research Unit, Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, P.O. Box 1906, Bellville 7530, South Africa; [email protected] (H.L.H.); [email protected] (T.E.M.) 2 Division of Haematology, Faculty of Health Science, University of Cape Town, Cape Town 7925, South Africa * Correspondence: [email protected]; Tel.: +27-21-959-6562; Fax: +27-21-959-6760 Received: 26 January 2020; Accepted: 26 March 2020; Published: 31 March 2020 Abstract: The expression of blood group antigens varies across human populations and geographical regions due to natural selection and the influence of environment factors and disease. The red cell membrane is host to numerous surface antigens which are able to influence susceptibility to disease, by acting as receptors for pathogens, or by influencing the immune response. Investigations have shown that Human Immunodeficiency Virus (HIV) can bind and gain entry into erythrocytes, and therefore it is hypothesized that blood groups could play a role in this process. The ABO blood group has been well studied. However, its role in HIV susceptibility remains controversial, while other blood group antigens, and the secretor status of individuals, have been implicated. The Duffy antigen is a chemokine receptor that is important in the inflammatory response. Those who lack this antigen, and type as Duffy null, could therefore be susceptible to HIV infection, especially if associated with neutropenia.
    [Show full text]