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Published in final edited form as: Vox Sang. 2018 Nov 12;114(1):95–102. doi: 10.1111/vox.12717

International Society of Blood Transfusion Working Party on Red Cell Immunogenetics and Blood Group Terminology: Report of the Dubai, Copenhagen and Toronto meetings.

Jill R Storry 1, Frederik Banch Clausen 2, Lilian Castilho 3, Qing Chen 4, Geoff Daniels 5, Greg Denomme 6, Willy A Flegel 7, Christoph Gassner 8, Masja de Haas 9, Catherine Hyland 10, Ji Yanli 11, Margaret Keller 12, Christine Lomas-Francis 13, Nuria Nogues 14, Martin L Olsson 1,15, Thierry Peyrard 16, Ellen van der Schoot 17, Yoshihiko Tani 18, Nicole Thornton 19, Franz Wagner 20, Christoph Weinstock 21, Silvano Wendel 22, Connie Westhoff 13, Vered Yahalom 23
PMCID: PMC6342652  NIHMSID: NIHMS989957  PMID: 30421425

Abstract

Background and objectives:

The International Society of Blood Transfusion (ISBT) Working Party for Red Cell Immunogenetics and Blood Group Terminology meets in association with the ISBT congress and has met three times since the last report: at the international meetings held in Dubai, United Arab Emirates, September 2016 and Toronto, Canada, June 2018; and at a regional congress in Copenhagen, Denmark, June 2017 for an interim session.

Methods:

As in previous meetings, matters pertaining to blood group antigen nomenclature and classification were discussed. New blood group antigens were approved and named according to the serologic and molecular evidence presented.

Results and conclusions:

Fifteen new blood group antigens were added to eight blood group systems. One antigen was made obsolete based on additional data. Consequently, the current total of blood group antigens recognised by the ISBT is 360, of which 322 are clustered within 36 blood groups systems. The remaining 38 antigens are currently unassigned to a known system. Clinically significant blood group antigens continue to be discovered, through serology/sequencing and/or recombinant or genomic technologies.

Keywords: blood groups, terminology, genetics

A key role for the Working Party on Red Cell Immunogenetics and Terminology is to review reports for blood group systems, antigens and associated blood group alleles. Historically, endorsement has occurred at the biennial ISBT International Congress. Curated blood group antigens and allelic tables are also reviewed by members in the interim who may also meet in the alternate years at regional congress meetings when there is a sufficient member quorum present.

A total of 15 blood group antigens were added to eight of the current blood group systems (Table 1). One antigen was made obsolete following additional investigation of the original antibody. This brings the current total of recognized blood group antigens to 360, of which 322 are clustered within 36 blood groups systems.

Table 1:

New antigens added to blood group systems

Blood Group System Antigen number Alt. name Prevalence Molecular basis Protein change Reference
MNS MNS49 JENU High GYPB; defined as an epitope within 38SYISSQTNGETG49 Interrupted by the amino acids encoded by the GYPA exon 3 insertion in the GP.Mur hybrid protein encoded by GYP*501. [1]
RH RH62 CEWA High RHCE c.114A>C RhCE p.Leu38Phe [2]
LU LU25 LUAC High BCAM c.662C>T BCAM p.Thr221Ile [3]
LU26 LUBI High BCAM c.1495C>T BCAM p.Arg499Trp [3]
LU27 LUYA High BCAM c.1184G>A BCAM p.Arg395His [4]
KEL KEL39 KEAL Low KEL c.877C>T Kell p.Arg293Trp [5]
YT YT3 YTEG High ACHE c.266G>A AChE p.Gly89Glu [7]
YT4 YTLI High ACHE c.169G>A AChE p.Gly57Arg [8]
YT5 YTOT High ACHE c.101G>A AChE p.Arg34Gln [8]
CROM CROM19 CROK High CROM c. 245T>C CD55 p.Leu82Pro [9]
CROM20 CORS High CROM c.713G>A CD55 p.Gly238Glu [10]
IN IN5 INRA High CD44 c.449G>A CD44 p.Arg150His [11]
IN6 INSL High CD44 c.276C>A CD44 p.His92Gln [12]
AUG AUG3 ATML Low SLC29A1 c.1159A>C SLC29A1 p.Thr387Pro [14]
AUG4 ATAM High SLC29A1 c.242A>G SLC29A1 p.Asn81Ser [15]
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Thus, there remain 38 serologically-defined antigens that have not been assigned to a blood group system. Fourteen of those reside in one of five collections (the 200 series), 17 in the low-prevalence series (700) and a further seven are in the 901 series (prevalence >90%).

New Blood Group Antigens

System 2: MNS

One antigen has been added to the MNS system, JENU (MNS49). An alloantibody to a high-prevalence antigen was shown by epitope mapping to be directed at the amino acids 38-SYISSQTNGETG-49 of glycophorin B (GPB). The antibody maker was a thalassemia patient of Thai origin who was shown to lack normal GPB, but who was homozygous for the GYP.Mur hybrid (GYP*501). Thus, JENU is a high-prevalence antigen on GPB that is absent from the GP.Mur hybrid [1]. The epitope defined above is interrupted in the hybrid protein. The name JENU combines JE, from the first two letters of the surname of the patient who made the JENU antibody, and NU, from the high frequency ‘N’ and U antigens present on GPB.

System 4: Rh

Identification of a new high-prevalence Rh antigen was made following the investigation of an antibody in the plasma of an elderly South African patient that was nonreactive only with Rhnull RBCs [2]. The patient’s RBCs typed as RH:‒51 however the antibody was not compatible with other examples of RH:‒51 RBCs. DNA sequence analysis revealed the nucleotide change RHCE c.114A>C that encodes a substitution of p. Leu38Phe in RhCE. The antigen has been assigned the name CEWA (RH62), with CE for RhCE and WA after the proband’s name.

Other RH:‒51 phenotypes are defined by the amino acid substitutions p.Gln41Arg (CW+) and p.Ala36Thr (CX+), and thus the RH51 epitope is likely defined by a peptide that includes amino acids 36–41 of RhCE. The incompatibility of the patient’s plasma with D-- RBCs suggests that CEWA is defined by an epitope shared by both RhD and RhCE, analogous to the G antigen.

System 5: Lutheran

Three high-prevalence antigens have been added to the Lutheran blood group system. An antibody in the plasma of a male patient of Maori origin was non-reactive with In(Lu) and Lu(a‒b‒) RBCs. Lutheran specificity was confirmed by the monoclonal antibody immobilisation erythrocyte assay (MAIEA), and subsequent DNA sequencing revealed a novel homozygous mutation c.662C>T in exon 6 of BCAM, encoding p.Thr221Ile in the Lu glycoprotein. This antigen has been named LUAC (LU25), LU for Lutheran and AC for Auckland, New Zealand [3].

The second antigen LUBI (LU26) (BI for Birmingham, United Kingdom) was identified following the investigation of multiple antibodies in a Caucasian woman with a history of transfusion. Her plasma contained anti-M, -Fya and -Jra as well as an unidentified antibody that was defined by MAIEA to be Lutheran-related. Sequence analysis of BCAM showed homozygosity for a novel mutation c.1495C>T in exon 12, encoding p.Arg499Trp [3].

Antibodies to an apparent high-prevalence Lutheran system antigen was identified in the plasma of two Turkish sisters during their respective pregnancies. Their RBCs were mutually compatible and subsequent molecular analysis of BCAM identified homozygosity for two nucleotide changes. The first is a synonymous change in exon 3, c.324G>A (p.Gly108Gly) known to be present in approximately 3–4% of the general population. The second one was found in exon 9, c.1184G>A, and predicts the amino acid change p.Arg395His on the fourth Ig superfamily domain of the Lutheran glycoprotein. The antigen was named LUYA (LU27) after the proposita [4].

System 6: Kell

A tragic neonatal death due to hemolytic disease led to the identification of an antibody to a novel low-prevalence antigen in the Kell blood group system [5]. The antigen, KEAL (KEL39; named after the proposita) was shown to be encoded by the substitution c.877C>T (p.Arg293Trp) in exon 8 of KEL, and inheritance could be demonstrated in three generations. KEAL is antithetical to the high-prevalence antigen, KHUL (KEL37) [6].

System 11: Yt

The Yt blood group system has more than doubled in size in the past three years. Use of recombinant protein reagents have been very helpful in teasing apart complex mixtures of antibodies, and three new high-prevalence antigens have been added to this system by Thornton and colleagues at the International Blood Group Reference Laboratory. In the first case, soluble recombinant Yt protein (srYt) successfully inhibited an additional unknown antibody to a high-prevalence antigen in plasma from an acute myeloid leukemia patient that contained anti-c, -Fyb and -Jkb. Subsequent sequence analysis of ACHE demonstrated homozygosity for the mutation c.266G>A in exon 2, encoding an amino acid change p.Gly89Glu in acetylcholine-esterase AChE) [7]. The new antigen is named YTEG (YT03) after the proband’s name.

An additional antibody to a high-prevalence antigen was found in the plasma of a pregnant woman with anti-Jka. Use of a recombinant soluble antigen panel demonstrated Yt specificity although the patient’s RBCs typed Yt(a+b-), YTEG+. ACHE sequencing confirmed the proband and her serologically compatible brother to be YT*A/A and revealed a novel homozygous mutation c.169G>A in exon 2, encoding p.Gly57Arg change in AChE. The antigen (YT04) has been named YTLI (after the referring centre in Liverpool) [8].

The third addition to the Yt blood group system followed the serological investigation of plasma from a young pregnant woman with sickle cell disease. Her plasma contained multiple antibodies, including anti-Fya, -Jsa and an antibody that reacted with all phenotypically similar RBCs. Again, reactivity with the latter was inhibited by srYt although antibodies to Yta, YTEG and YTLI were excluded. Sequencing of ACHE identified a novel homozygous mutation c.101G>A in exon 2, encoding p.Arg34Gln change in AChE. The antigen (YT05) has been named YTOT, also after the referring laboratory [8].

System 21: Cromer

A novel Inab-like phenotype has been molecularly characterised after an antibody that was compatible only with IFC-negative RBCs was identified in the plasma of a Druze woman. Her RBCs typed negative with all available antisera to Cromer blood group antigens and were nonreactive with anti-CD55 by flow cytometry. Molecular analysis of CD55 revealed the mutation c.245T>C, which changes p.Leu82Pro. The WESb antigen is defined by Leu82, and the antithetical low-prevalence antigen WESa is defined by c.245T>G (p.Leu82Arg). Thus, this is the third polymorphism at this nucleotide position. Interestingly, Wes(a+b‒) RBCs were weakly incompatible with the patient’s plasma indicating that the absence of p.Leu82 was insufficient for compatibility, and suggested that p.Leu82 encodes for both WESb and for another high-prevalence antigen. The antigen (CROM19) has been named CROK after the patient [9].

Exome sequencing was used to resolve an unidentified antibody to a high-prevalence antigen in the plasma of a 103-year old woman of French Corsican descent. Her history showed a single pregnancy in 1949 and the antibody was first detected in 2002. When new samples were received for investigation in 2016, DNA was isolated and exome sequenced, which revealed homozygosity for c.713G>A in exon 6 of the CD55 gene, predicted to cause a p.Gly238Glu amino acid change. Her son was found to be heterozygous for the same mutation. Cromer specificity of the antibody was subsequently confirmed when RBCs of the Inab phenotype became available. The antigen (CROM20) was named CORS to reflect the patient’s origin [10].

System 23: Indian

INRA (IN5) is a new high-prevalence antigen in the Indian blood group system, and was named after the patient. The defining antibody was present in the plasma of a female patient from Surat in the Indian state of Gujarat and demonstrated the classic absence of reactivity with papain-treated RBCs characteristic of Indian blood group system antibodies. The antibody was compatible only with the RBCs of the patient’s brother. Sequence analysis of CD44 demonstrated homozygosity for a novel homozygous synonymous mutation c.255C>T in exon 3 (p.His85His), and for a novel homozygous missense mutation c.449G>A in exon 5, encoding p.Arg150His [11].

Soluble recombinant CD44 helped to resolve the identity of an antibody to a high-prevalence antigen in the plasma of a Sri Lankan patient with suspected In specificity. Both the patient and his serologically compatible brother typed In(a−b+), INFI+, INRA+. Sequencing of CD44 revealed homozygosity in both siblings for a mutation c.276C>A, which predicts an amino acid change p.His92Gln. The antigen (IN6) has been named INSL to reflect the origin of the patient [12].

System 36: Augustine

The Augustine system continues to expand since its discovery in 2015 [13]. A case of severe HDFN led to the discovery of a low-prevalence antigen that was shown by targeted exome sequencing to be encoded by SLC29A1. DNA from both the infant and father revealed a mutation c.1159A>C, in exon 12 predicting an amino acid change of p.Thr387Pro. In an extended family study, six paternal family members carried the nucleotide substitution; red cells from these six members showed incompatibility with the mother’s plasma, demonstrating that serological reactivity segregated with the mutation. The predicted amino acid change is four amino acids from the amino acid that defines the Ata antigen in the fifth extracellular loop. The antigen (AUG3) was named ATML after the initials of the patient [14].

A novel high-prevalence antigen in this system was defined in a follow-up investigation of a long-time unresolved antibody in a female patient. Targeted exome sequencing in this case revealed homozygosity for c.242A>G in the SLC29A1 gene, that changes p.Asn81Ser. Confirmatory serology showed that the plasma was compatible with AUG:−1 RBCs, which are the null phenotype in this blood group system. The antigen (AUG4) was named ATAM. after the proband’s name [15].

Other changes to blood group systems

System 28: GLOB

When PX2 was assigned to this blood group system, it was moved from the GLOB collection (see below) into the GLOB blood group system and assigned the number GLOB2 (028002) [16]. This has caused confusion with old records of rare red blood cells in some laboratories, thus the decision was taken to reassign PX2 as GLOB4, and the numbers GLOB2 and GLOB3 have been made obsolete. A current list of obsolete numbers is shown in Table 2.

Table 2:

Obsolete numbers for blood group antigens organized by blood group system, collections (200 series), low-prevalence antigens (700 series) and high-prevalence antigens (901 series).

Obsolete
number		 Symbol or
previous symbol		 Subsequent number
(Current number in bold)		 Year reported
obsolete		 Obsolete
number		 Symbol or
previous symbol		 Subsequent number
(Current number in bold)		 Year reported
obsolete
Antigens in blood group systems Antigens in collections
001005 H 018001 1991 Collection 201 GE System 020 1991
003002 P 209001 1991 Collection 202 CROMER System 021 1991
003003 Pk 209002 1991 Collection 203 IN System 023 1995
004013 RhA 1995 Collection 204 AU 1991
004014 RhB 1995 204001 Aua 005018 1991
004015 RhC 1995 204002 Aub 005019 1991
004016 RhD 1995 205003 Yka 022005 1993
004024 ET 1995 205004 Kna 022001 1993
004025 LW 1985 205005 Knb 022002 1993
004038 Duclos 901013 1995 205006 McCa 022003 1993
005010 Singleton 1991 205007 Sla 022004 1993
005015 AnWj (Anton) 901009 1991 Collection 206 Gregory 1993
006008 Kw 1991 206001 GY1/Gya 014003 1993
006009 KL 1985 206002 GY2/Hy 014004 1993
006015 Kx 019001 1991 207001 I 027001 2003
008004 FY4 2010 Collection 209 GLOB 2018
016001 LW1 phenotype 1985 209001 P 028001 2003
016002 LW2 phenotype 1985 209002 Pk 003003 2010
016003 LW3 phenotype 1985 209003 LKE 901017 2018
016004 LW4 phenotype 1985 209004 PX2 028002 2014
020001 Ge1 1991 Collection 211 WR 1995
030004 RHAG4 2018 211001 WR1/Wra 010003 1995
211002 WR2/Wrb 010004 1995
Collection 212 Vel/ABTI 2014
212001 Vel 034001 2014
212002 ABT1 901015 (reverted) 2014
Antigens in the low-prevalence (700) series Antigens in the low-prevalence (700) series
700001 Wra 010003 1991 700035 Tcb 021003 1991
700004 Swa 010013 1999 700036 Tcc 021004 1991
700007 Lsa 020006 1991 700037 NFLD 010016 1999
700008 Tra 010019 2004 700038 Hov (= Wu) 010019 1999
700009 Wb 020005 1991 700041 SW1 010021 2001
700010 Bpa 010010 1999 700042 WES (WESa) 021008 1991
700011 Or 002031 2008 700046 BOW 010015 1999
700012 Gf 1991 700048 FPTT 004050 1995
700013 Wu 010009 1999 700051 ELO 010008 1999
700014 Jna 010017 1999 700053 LOCR 004055 2003
700015 Rd 013004 2003 700055 WARR 010007 1996
700016 Heibel 1990 700052 SARA 004047 2014
700020 Ana 020007 1991
700022 Moa 010011 1999 Antigens in the high-prevalence (901) series
700023 Hey 1995 901001 Vel 212001 2004
700024 Rla (= Lsa) 020006 1991 901002 Lan 033001 2012
700025 Ina 023001 1995 901003 Ata 036002 2015
700026 Fra 010020 2001 901004 Joa 014005 1993
700027 Rba 010006 1996 901005  Jra 032001 2012
700029 Vga 010013 1999 901006 Oka 024001 1999
700030 Wda 010005 1996 901007 JMH 026001 2001
700031 Dha 020008 1991 901010 Wrb 010004 1991
700032 POLL 1991 901011 MER2 025001 1999
700033 Osa 002038 1995 901013 Duclos 030001 2008
700034 Hga 010012 1999 901015 ABTI 212002 2004
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System 30: RHAG

Two independent investigations have shown that the polymorphism RHAG c.808G>A (p.Val270Ile) does not encode a low-prevalence antigen as first described. In a study of RHD, RHCE and RHAG variation examined by whole exome sequencing of samples from children with sickle cell disease, Chou et al. have shown this polymorphism to be common, with 14.6% of samples demonstrating heterozygosity [17]. Supplementary serological investigation of the original sample, reported following a case of severe hemolytic disease of the fetus and newborn (HDFN) [18], revealed the antibody to be anti-sD (MNS23). Consequently, RHAG4 has been made obsolete.

Changes to the Collections (200), Highs (901) and Lows (700) series

The GLOB collection

The discovery of genetic basis for the GLOB blood group system resulted in the assortment of antigens previously defined as the GLOB collection being placed in the GLOB blood group system. However, since the high-prevalence antigen, LKE remained the only antigen in the GLOB collection, the decision was made to move LKE to the 901 series until the molecular basis is identified. It has been assigned the number 901017. Accordingly, the GLOB collection has been made obsolete.

Gene terminology and conclusion

Clinically significant blood group antigens continue to be discovered, through serology/sequencing and/or recombinant or genomic technologies.

The Working Party continues to update the blood group antigen tables and the allele nomenclature tables. These can be found on the ISBT website.(http://www.isbtweb.org/working-parties/red-cell-immunogenetics-and-blood-group-terminology/) We are working actively with the Locus Genome Reference initiative (https://www.lrg-sequence.org/) to qualify reference sequences for all genes encoding blood group systems. This work in on-going.

Acknowledgements

Since the last report [16], Dr Joann Moulds and Dr Geoff Daniels resigned from the Working Party. We sincerely thank them for everything they have done for the Working Party over many years. We especially thank Geoff for his leadership from 1993 to 2010.

Funding

CAH is funded by the Australian Red Cross Blood Service and acknowledges the Australian Governments that fund the Blood Service for provision of blood, blood products and services to the Australian Community. WAF is supported by the Intramural Research Program (project ID Z99 CL999999) of the NIH Clinical Center. TP is supported by the Laboratoire d’Excellence GR-Ex for exome sequencing studies and especially acknowledges Pr Olivier Hermine, Head of this consortium.

Appendix 1. Current members of the Working Party for Red Cell Immunogenetics and Blood Group Terminology

Dr Jill R Storry (Outgoing chair): Dept. of Clinical Immunology and Transfusion Medicine, Office for Medical Services, Lund, Sweden. jill.storry@med.lu.se

Dr Frederik Banch Clausen: Dept. of Clinical Immunology, Copenhagen University Hospital, Copenhagen, Denmark. frederik.banch.clausen@regionh.dk

Prof Dr Lilian Castilho: University of Campinas/Hemocentro, Campinas, Brazil. castilho@unicamp.br

Dr Qing Chen: Jiangsu Province Blood Center, Nanjing, Jiangsu, China. qngchen@gmail.com

Prof Dr Masja de Haas: Sanquin Blood Supply Foundation, Amsterdam, The Netherlands. m.dehaas@sanquin.nl

Dr Greg Denomme: Blood Center of Wisconsin, Milwaukee, WI. greg.denomme@bcw.edu

Prof Dr Bill (W) A Flegel: Department of Transfusion Medicine, NIH Clinical Center, National Institutes of Health, Bethesda, MD, USA. flegelwa@cc.nih.gov

Dr Ji Yanli: Institute of Clinical Blood Transfusion Guangzhou Blood Center, Guangzhou, People’s Republic of China: jiyanli2013@163.com

Dr Christoph Gassner (current Co-Chair): Blutspende Zurich, Zurich, Switzerland.c.gassner@zhbsd.ch

Dr Catherine Hyland (current Co-Chair): Australian Red Cross Blood Services, Brisbane, Australia. chyland@arcbs.redcross.org.au

Dr Margaret Keller: American Red Cross Blood Services, Philadelphia, PA. Margaret.Keller@redcross.org

Ms Christine Lomas Francis: New York Blood Center, New York, NY, USA. clomas-francis@nybc.org

Dr Nuria Nogues: Banc de Sang i Teixits, Barcelona, Spain. nnogues@bst.cat

Prof Dr Martin L Olsson: Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden. Martin_L.Olsson@med.lu.se

Dr. Thierry Peyrard, Institut National de la Transfusion Sanguine, Département Centre National de Référence pour les Groupes Sanguins ; UMR_S1134 Inserm Université Paris Diderot ; Laboratoire d’Excellence GR-Ex, Paris, France. tpeyrard@ints.fr

Prof Dr C Ellen van der Schoot: Sanquin Research at CLB, Amsterdam, The Netherlands. e.vanderschoot@sanquin.nl

Dr Yoshihiko Tani: Japanese Red Cross Kinki Block Blood Center, Ibaraki-shi Osaka, Japan. y-tani@kk.bbc.jrc.or.jp

Ms Nicole Thornton: International Blood Group Reference Laboratory, NHS Blood and Transplant, Bristol, UK. nicole.thornton@nhsbt.nhs.uk

Dr Franz Wagner, Red Cross Blood Service NSTOB, Springe, Germany. fwagner@bsd-nstob.de

Dr Christoph Weinstock: German Red Cross Blood Service, Bade-Wurttemberg-Hessen, Ulm, Germany.

c.weinstock@blutspende.de

Dr Silvano Wendel: Blood Bank, Hospital Sirio-Libanes, São Paulo, Brazil. snwendel@terra.com.br

Dr Connie M Westhoff: New York Blood Center, New York, NY cwesthoff@nybc.org

Dr Vered Yahalom: Rabin Medical Center, Petach Tiqva, Israel. Veredya2@clalit.org.il

Footnotes

Conflict of Interest declaration

There are no conflicts of interest to declare with regard to the data reported in this paper.

Statement of Disclaimer.

The views expressed do not necessarily represent the view of the National Institutes of Health, the Department of Health and Human Services, or the U.S. Federal Government.

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