G. L. Daniels (Chair) D. J. Anstee, J. I? Cartron ctl Dahr; I? D. Issitt 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

International Society of Blood Transfusion Societe lnternationale de Transfusion Sanguine Section Editor: H. Gunson, Manchester

Vox Sang 1995;69:265-279

Blood Group Terminology 1995 ISBT Working Party on Terminology for Red Cell Surface Antigens

Since the first human blood groups were discovered al- most a century ago, many hundreds of new red cell antigens have been identified. Because of the extended time period over which these antigens were discovered, a variety of dif- 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 a numerical notation was introduced (Fy3). Some antigens were given different names in different laboratories, based on alternative genetic theories (D and Rho).

In 1980 the International Society of Blood Transfusion (ISBT) established a Working Party to devise a genetically based numerical terminology for red cell surface antigens. In 1990 the Working Party published a monograph describ- ing a numerical terminology for 242 red cell antigens [I], and brief updatings followed in 1991 [2] and 1993 [3]. In the 6 years since the 1990 report many amendments to the clas- sification have been necessary: 18 new antigens have been identified and 6 others declared obsolete due to lack of suit- able reagents; four new systems have been created (all from existing collections); the Auberger antigens joined the Lutheran system; the Gregory antigens and Jo” joined the Dombrock system; the Wright antigens joined the Diego system. Furthermore, since, 1990, many of the blood group genes have been isolated: of the genes controlling the 23 systems, only four (PI, JK, SC, DO) remain to be cloned.

The purpose of this monograph is to describe the ISBT terminology for red cell surface antigens and to tabulate the complete 1995 version of the classification. In addition, an alternative ‘popular’ terminology is suggested in an attempt to reduce the number of different names used in publica-

tions on red cell antigens. Much of the information provided in the 1990 monograph [l] is reiterated here so that referral back will not generally be required, but only references after 1990 are provided.

ISBT Numerical Terminology

The mandate of the Working Party is to provide a termi- nology for red cell surface antigens. By definition, these an- tigens must be defined serologically by the use of a specific antibody. Numerical designations and blood group symbols cannot be allocated to nucleotide or amino acid sequences, or to restriction fragment length or other DNA polymor- phisms, even though the presence of specific blood group antigens may be signposted by these techniques. All anti- gens receiving ISBT numbers must have been shown to be inherited characters.

All authenticated antigens fall into one of 4 classifica- tions: systems; collections; low incidence antigens (700 se- ries), and high incidence antigens (901 series). A blood group system consists of 1 or more antigens controlled at a single gene locus, or by 2 or more very closely linked ho- mologous genes with little or no observable recombination between them. Each system has been shown to be genetical- ly discrete from every other system. Collections consist of serologically, biochemically, or genetically related antigens which do not fit the criteria required for system status. The 700 and 901 series contain low and high incidence antigens, respectively, which cannot be included in a system or col- 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 5 N D ( U K )

Each antigen belonging to a blood group system is iden- tified by a 6-digit number (table 1-3). The first 3 digits rep- resent the system (e.g. 006 for Kell), and the second 3 the specificity (e.g. 006003 for Kp"). Alternatively, the system symbol followed by the antigen number may be used (e.g. KEL003 or, more usually, KEL3 as sinistral zeros may be removed). Phenotypes are represented by the system sym- bol, followed by a colon, followed by a list of antigens sep- arated by commas. Those antigens shown to be absent are preceded by a minus sign (e.g. KEL:-1,2,-3,4). Genes are

Table 1. Examples of antigen, phenotype, gene, and genotype des- ignations in the traditional and ISBT terminologies

Traditional ' ISBT

Antigen Lu" 005001 or L U I

Gene Lu" LU I Lu LUO

Lu" Lu'/Lu'' L d J LU 1.8/2,14 la'' LllC'/LU

Phenotype Lu(a-b+) LU:-I, 2

Gcnotypc Lu" L~lii L u 2/2

L u 2, K/O

' And 'popular' alternative

designated by the system symbol, followed by a space (or asterisk), followed by the antigen number (e.g. KEL 3). Gc- notypes have the system symbol, followed by a space (or asterisk), followed by alleles or haplotypes separated by a slash (e.g. KEL 2,3/2,4). Amorph or null genes are repre- sented by a 0 (e.g. KEL 2,3/0). Gene and genotype desig- nations are italicized (or underlined). Antigen, phenotype, gene, and genotype designations for collections are con- structed in the same way. For the 700 and 901 series, 700 or 901 replaces the system symbol.

Symbols for Gene Loci

The symbol for a gene or cluster of genes controlling a blood group system is the italicized symbol for the system (e.g. CO for the gene controlling the Colton system). How- ever, the genes controlling most of the blood group systems have been cloned and in many cases the gene locus has an alternative symbol (table 2), usually because the protein product of the gene is of known function or the gene had an existing symbol before the association with the blood group was known. Examples: the gene controlling expression of 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 1 002 003 004 005 006 007 008 009 010 01 1 012 013 014 015 016 017 018 019 020 02 1 022 023

ABO M N S P Rh Lutheran Kell Lewis Duffy Kidd Diego Yt

Scianna Dombrock Colton Landsteiner-Wiener ChidoIRodgers Hh Kx Gerbich Cromer Knops Indian

x g

ABO MNS PI RH LU KEL LE FY JK DI YT XG SC DO CO LW CHIRG H XK GE CROM KN IN

ABO GYPA, GYPB, GYPE PI RHD, RHCE LU KEL FUT3 FY .JK AEI ACHE XG sc DO AQPl LW C4A, C4B FUTI XK GYPC DAF CR 1 CD44

9q34.1Lq34.2 4q28-q3 1 22q 1 1.2-qter lp36.2-~34 19q12-q 13 7q33

1 q22-q23

17q 12-q2 1

19~13 .3

18ql I-qI2

7q22 Xp22.32

Not known 7p14 19~13.2-cen 6p2 1.3

1 p36.2Lp22.1

19q13 xp21.1 2q 14-q2 1

I lp13

1 q32 1 q32

4 1 1 5-8 9 10-12 13-1 7 18- 22 23 24-26 27-29 30,3 1 1

32,33 34 I 35,36 37 I I 38.39 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" C l a 003 P P1

~~

~~~ ~~- ~. ... ... ~.

... 004 RH--- . D C E c e _ f Ce C" Cx V E" G ... ... ... Hr,, 005 LU __ L U ~ Luh Lu3 Lu4 Lu5 Lu6 Lu7 Lu8 Lu9 . . . L u l l 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 D I Did Dih Wr" Wrh 011 YT Yt" Yth

~~~~

~ _ _ _ 015 CO _ c o d Coh Co3

017 CH/RG Chl Ch2 Ch3 Ch4 Ch5 Ch6 WH Rgl Rg2

0 T X K ~ Kx

016 LW ... ... ... .. Lwa LW'b LWh

r H - H

~~

~- 020 GE . . Ge2 Ge3 Ge4 Wb Ls" Ana Dh" ~- T C R O M C f Tcd Tch Tc' Drd Esa IFC WESa WESh UMC

023 IN- Ina Inh Kn" Knh McC" SId Yk" _____ 022 KN-

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 AQf 1, the gene producing a water transporter Aquaporin 1 [33]; presence of H antigen on the red cells is determined by an cxl,2-fucosyltransferase gene, FUTl [35], and presence of Lewis antigens on red cells is indirectly determined by an ( x 1,3/4-fucosyltransferase gene, FUT3 [13]; at least 2 genes govern the Rh antigens and are called RHD and RHCE. The symbol for the gene governing a serologically determined blood group antigen comprises the system symbol and anti- gen number (e.g. RHl,DZ2, CO I). When the gene encoding a blood group antigen is determined by non-serological means, such as RFLP analysis or nucleotide sequencing, the altcrnative symbol should be used (e.g. AEI instead of DI, and IIAF instead of CROM) and allele designations should conform with the established terminologies employed for RFLPs or point mutations [40,41].

A 'Popular', Alternative Terminology

The numerical terminology was devised primarily for computer storage of information on blood group antigens and to provide a framework for a genetical classification of blood group antigens. The numerical terminology is not suitable for everyday communication and many scientists working in the field of human blood groups prefer not to use it in publications. This has led to a variety of alternative names being used for some blood group antigens. In an at- tempt to introduce some uniformity, a recommended alter- native notation is provided in table 3. In most cases this is identical to the original published name or symbol, but in a few the notation in more common usage is provided. For example, in system 13 (Scianna), the old names Sm and Bu" have been replaced by Scl and Sc2, respectively, and in sys- tem 6 (Kell) K11 and K17 have replaced Cote and Wk" for these antithetical antigens. The original symbols of those antigens whose names have been changed are as follows: RH29 = 'total Rh'; RH33 = Har; RH42 = Cce'; LU3 = Lu"; LU9=Mull; LU12=Much; LU13=Hughes;KELll=Cote; KEL12 = B0c; KEL14 = San; KEL16 = 'k-like'; KEL17 =

Wk"; KEL19 = Sub; KEL24 = CIS; JK3 = Jk"; SCl = Sm; SC2 = Bu".

Blood Group Systems

There are currently 23 systems containing a total of 194 antigens (table 2,3). The DO locus alone remains to be allo- cated to a chromosome.

Modifications since 1990: Existing Systems 002, The MNS System. Six new antigens have been add-

ed, all of low incidence. MNS32 (DANE) is associated with a glycophorin A (GPA) molecule containing a short insert derived from the pseudoexon of the glycophorin B (GPB) gene, GYPB [42, 431. This GP(A-B-A) structure also ex- presses MNSlO (Mur). MNS33 (TSEN) and MNS34 (MI- NY) represent abnormal amino acid sequences on GP(A-B) hybrid molecules resulting from a GPA-58 to GPB-27 .junc- tion; MNS33 is only expressed when the GPB portion of the molecule expresses S [44,45], whereas MNS20 (Hil) is as- sociated with the s-specific sequence. MNS35 (MUT) is an antigen defined by antibodies which generally behave as in- separable anti-MNS10 and anti-MNS19 (anti-MuriHut), al- though a few exceptional phenotypes demonstrate that more than simple cross-reactivity is involved [46] At pre- sent, there is controversy over whether MNS7 (Mi") should be declared obsolete and whether the nomenclature of the Miltenberger subsystem should be continued [46, 471. MNS36 (SAT) [48] is associated with an abnormal glyco- phorin sequence arising from either a GP(A-B) hybrid in- volving a GPA-71 to GPB-40 junction or from a GPA mole- cule with a 3 amino acid insert from GPB (GPB-40 to GPB-42) between GPA-71 and GPA-72 [49, 501. MNS37 (ERIK) is located on a GPA molecule with a Gly-59-Arg substitution; exon skipping within the abnormal GYPA also results in a shortened GPA expressing MNS15 (St') [51,52]. In one family, MNS37 and MNS15 are associated with a GPA molecule lacking the product of exon 3 of GYPA be- cause of the insertion of an inactive splice site from a GYPE gene [53]. MNS38 (Osa, previously 700033) was shown to be located on GPA by immunochemical techniques [54].

The Working Party recognises that MNS8 (M') and MNS30 ('N', the trypsin resistant N antigen on GPB) should not have received numbers since they are not anti- gens recognised by specific antibodies. However, these numbers will remain since the determinants they represent are very well defined immunologically and biochemically.

004, The Rh System. Three new antigens have been add- ed, two of low incidence and one of high incidence. The assignment to the Rh system of RH49 (STEM), which may be associated with the absence of RH19 (hr') or RH31 (hr''), is supported by family evidence (lod score = 5.21 at t3 = 0) [55]. Family information (lod score = 4.12 at 8 = 0) was also responsible for the elevation of 700048 (FPTT) to RH50, an antigen associated with unusual DCe and Dce (with RH33) complexes, and, in some examples, with a partial RHl (D) antigen (DFR) [56, 571. The high incidence antigen RH51 (MAR) has an antithetical relationship with RH8 (C") and RH9 (C") (lod score = 10.76 at 0 = 0) [58].

268 ISBT Working Party Blood Group Terminology 1995

Five Rh antigens, RH13 (RHA), RH14 (RhB), RH15 (Rh‘), RH16 (RhD), and RH24 (ET) have been declared ob- solete as the reagents essential for their definition are no longer available.

005, The Lutherun System. The Auberger antigens (pre- viously collection 204) joined the Lutheran system and be- came LUIS (Ad) and LU19 (Aub) based on the following evidence: location on the Lutheran glycoproteins [59]; gene location at 19q13.2 [60], and genetic linkage studies of fam- ilies informative for LUI, LU2, and the Auberger polymor- phism (lod score = 10.83 at 8 = 0) [61]. Retesting of a family revoked the only evidence against the Auberger antigens belonging to the Lutheran system [62].

A high incidence antigen absent from cells of the Luth- eran-null phenotypes and located on the Lutheran glycopro- teins is numbered LU20 [63].

010, The Diego System. Expression of DI1 (Di’) or D12 (Dib) is determined by Leu-854 and Pro-854, respectively, of AEI, the anion exchanger (band 3) [25]. Demonstration that WRl (Wr’) and WR2 (Wrb) of collection 211 are deter- mined by Lys-658 or Glu-658, respectively, of AE1[26] led to WRI becoming D13, WR2 becoming DI4, and abolition of collection 211. D14 requires the presence of Arg-61 of GPA for expression [26].

014, The DombrockSystem. Serological and biochemical evidence has led to the antigens of collection 206 (Gregory) and the high incidence antigen 901004 (Jo’) becoming part ofthe Dombrock system [64]. GYI (Gy’) has become D03; GY2 (Hy) is D04; 901004 is D05. Red cells lacking DO3 represent a null phenotype and are D0:-1,-2,-3,4,-5. D O : 4 cells are DO:-1,2,3 with weak DO2 and D03. D01, D03, D04, and DO5 have all been shown to be on the same membrane glycoprotein [64,65].

Modifications since 1990: New Systems Three collections and part of a fourth have made up 4

new blood group systems. 020, The Gerbich System. Demonstration of recombina-

tion between GYPC and DI, DO, and Y7: using a Tug1 RFLP of GYPC, meant that Gerbich was genetically discrete from all other existing systems [66]. Consequently collection 201 was reclassified as system 20.

Two new low incidence antigens were added to the Ger- bich system. GE7 (And previously 700020), expressed on GPD but not GPC, results from a point mutation within GYPC which causes an Ala-23-Ser substitution in GPC and an Ala-2-Ser substitution in GPD [67]. GE8 (Dh”, previous- ly 700031), expressed on GPC, results from a Leu-14-Phe substitution in GPC [68].

021, The Cromer System. Cromer antigens are located on the complement regulatory molecule, decay accelerating factor (DAF). Cromer (previously collection 202) became a system when DAF was shown to be distinct from loci con- trolling all other blood group systems [69]. For conve- nience, the symbol for system 21 has been abbreviated from CROMER to CROM.

022, The Knops System. Five antigens from collection 205 (Cost) comprise the Knops system. These antigens, KNI (Kn’)), KN2 (Knb), KN3 (McC”), KN4 (SP), and KN5 (Yk“), are located on the C3b/C4b receptor, CR1 [38, 391. The CRI locus belongs to the regulators of complement ac- tivation (RCA) gene cluster on chromosome lq32, which also includes DAE: the Cromer locus. Therefore, like DAE CR1 is distinct from loci controlling all other systems. The antigens COST1 (Csa) and COST2 (Csb) do not appear to be on CR1 and remain in the Cost collection (205) [39,70].

023, The Indian System. IN1 (Ina) and IN2 (Inb), previ- ously of collection 203, are located on the lymphocyte hom- ing receptor CD44. The CD44 locus is on chromosome llp13, which distinguishes it from all blood group system loci except DO. As the Dombrock system antigens are not located on CD44 [64], Indian became system 23.

Guidelines for the Establishment of New Blood Group Systems Either of the following criteria must be met. (1) an anti-

gen whose production is governed by a ‘polymorphic’ gene that is distinct from the genes involved in the established systems, or (2) an antigen whose production is governed by a non-polymorphic gene of known chromosomal assign- ment that is distinct from the genes involved in the estab- lished systems.

All established blood group systems meet these criteria.

Guidelines for the Inclusion of a New Specijkity in an Established System At least one of the following four criteria must be met.

All antigens awarded an ISBT number must have been shown to be inherited. (1) an antithetical relationship be- tween a new antigen and one already assigned to a system; (2) demonstration that expression of the antigen is associ- ated with a variation in the nucleotide sequence of the gene controlling a system; (3) evidence, from a linkage analysis of family data, that the controlling allele is probably a newly recognised form of the pertinent gene, and supporting ser- ological or biochemical data; or (4) demonstration that an antigen is located on a protein or glycoprotein which carries other antigens belonging to a system. It must be remem- bered, however, that this could result from post-translation-

269

Collection Antigen Connection

No. name symbol No. symbol incidence sero- bio- genetic % logical chemical

205 Cost COST 205001 Cs" 95 X

205002 Csb 34 X

207 11 1 207001 I > 99 X X

207002 i

208 Er ER 208001 Er" > 99 X

208002 Erb < 1 X

209 GLOB0 209001 P > 99 X X

209002 Pk * X X

209003 LKE 98 X

* X X ~ _ _ ~ _ _ _ _ _ ~ ~

__

Table 4. Collections of antigens

210 210001 LeC 1 210002 Led 6

X X X X

*By standard serological tests, may appear to be low incidence. Obsolete collections: 201 Gerbich; 202 Cromer; 203 Indian; 204 Auberger; 206 Grcgory;

21 1 Wright.

al modification of a gene product, such as glycosylation, which would not support inclusion within the system.

Blood Group Collection (table 4)

Of the 9 collections devised in 1990 [I], and the 2 added in 1991 [2], 6 have now become obsolete: 201 (Gerbich), 202 (Cromer), and 203 (Indian) have become systems, and the antigens of collections 204 (Auberger), 206 (Gregory), and 211 (Wright) have been incorporated into systems 005 (Lutheran), 014 (Dombrock), and 010 (Diego), respectively. Five of the seven antigens of collection 205 (Cost) now comprise system 022 ( h o p s ) .

vide the statistically significant evidence required for their inclusion. Another Rh-associated antigen, FPTT, was given the number 700048 in 1991 [2], but has now become RH50 on the basis of pedigree evidence [57]. Six other 700 num- bers have been declared obsolete since 1990: 700012 (0, 700023 (Hey), and 700032 (POLL) because suitable re- agents are no longer available for their definition; 700001, 700020, 700031, and 700033 have been incorporated into blood group systems (table 7).

Criteria for Inclusion in the 700 Series. ( I ) lncidence of <I% in most populations tested; (2) distinction from all other numbered low incidence antigens of the 700 series as well as those of the blood group systems and collections, and (3) demonstration of inheritance through at least 2 gen- erations.

700 Series, Low Incidence Antigens (table 5) 901 Series, High Incidence Antigens (table 61

There are currently 37 antigens in the 700 series (ta- ble 5). Since 1990,6 new antigens have been added, 700049 to 700054. All have been shown to be distinct from all other 700 series antigens. Two ofthese antigens, 700050 (HOFM) and 700053 (LOCR), are serologically related to system 4 (Rh): 700050 is associated with depressed RH2 (C) in the only family in which it has been detected [74] and 700053 is transmitted with altered expression of RH4 (c) in 2 of the 3 families studied [77]. Family analyses neither exclude these 2 antigens from belonging to system 4 (Rh), nor pro-

The 901 series was created in 1990 to replace the 900 series of high incidence antigens, which was severely de- pleted by the introduction of the blood group collections. Only one antigen, 901014 (PEL) [82], has been added since (table 6). 901014 is distinct from all other high incidence an- tigens and the antigen negative phenotype was shown to be inherited in one family. Two 901 numbers are now obsolete: 901005 (Joa) and 901010 (Wrb) have become part of blood group systems (table 7).

270 ISBT Working Party Blood Group Terminology 1995

Table 5. The 700 series: Low incidence antigens

No. Name Symbol Exluded from systems Ref. No. Name Symbol Exluded from systems Ref.

700002 700003 700004 700005 700006 700008 7000 10 7000 I3 7000 I4 7000 15 7000 17 7000 18 7000 19 70002 1 700022 700026 700027 700028 700029 700030

Batty Christiansen Swann Biles Box Travcrsu Bishop Wulfsberg Nunhart Radin Torkildsen Peters Reid Jensen Moen Froese Redelberger Livesay Van Vugt Waldner

BY Chrd SW"

Bi Bx" Tr"

wu Jnd Rd To" Pt'' Red Je" Mo" Fr" Rb" Li"

Wdd

BP"

Vg.1

I , 4-6, 8, 19 2, 12, 19

4, 12, 19 1,4, 8, 12, 19 14 ,8 , 9, 12, 19 14, 8,9, 12, 19

2 4 , 6 , 8,9, 12, 19 1-12,14-23' 2 4 , 6, 8,9, 12, 17, 19

1-9, 11-14, 16-19

1-5, 8,9, 12, 17, 19

1-5, 8,9, 12, 19 I , 2,4-6,8,9, 12, 19 1,2,4,5 1,2,4,8,9, 12, 19

1 4 , 6 , 8,9, 12, 19 2,4, 12, 192 2 1-9,11-17, 19

1-9,11-17,19

71

72

700034 Hughes Hg" 700037 NEW- NFLD

FOUNDLAND 700039 Milne 700040 Rasmussen RASM 700041 SWI 700043 Oldeide 01" 700044 JFV 700045 Katagiri Kg 700046 Bowyer BOW 700047 Jones JONES 700049 HJK 700050 HOFM 70005 1 E L 0 700052 SARA 700053 LOCR

700054 RElT 700055 Warrior WARR

2,4, 12, 19 1-3,8,9,11,12,19

2,6, 8, 12, 19 2,3,7,8, 12, 19

1-4,9,12, 19' 2,4,5,8,9, 12, 19 10, 12, 19 1 4 , 6 I , 2, 8, 1 I , 12, 19 12,19 73 2,8, 12, 194 74 2,4,5, 8,9, 12, 14, 15, l9,20 75 8,9 76 1,2, 5,6, 8,9, 11, 15, 77 16, 204 1,2,4,8, 12, 19 78 2, 5, 7-9, 12, 17, 19,20 79

~~

I

' '

Chromosomal location and biochemical information suggest that 700.15 belongs to system 13 (SC), but the evidence is inconclusive. One family provides a suggestion of linkage to LU(lod score 1.204 at 8 = 0). Serological association with system 4 (RH), but shown to be genetically discrete. Serological association with system 4 (RH), inadequate family data to permit membership of that system.

Criteriu,for Inclusion in the 901 Series. (1) Incidence of >90% in most populations tested; (2) distinction from all other numbered high incidence specificities, and ( 3 ) dem- onstration that the antigen is lacking from the red cells of at least 2 sibs, i.e. that the negative phenotype is genetically determined.

Obsolete Numbers (table 7)

There is no recycling of blood group numbers: once a number has been allocated to a specificity, that number can- not be subsequently used for any other specificity. Conse- quently, if the number of a specificity becomes inappropri- ate, then that number becomes obsolete. Obsolete numbers are listed in table 7. Some numbers become obsolete be- cause defining reagents cease to be available, others be- come obsolete when the status of the antigen changes. For example, the low and high incidence antigens 700001 (Wr") and 901010 (Wrh) became 211001 and 211002 ofthe Wright collection because of their antithetical relationship and then 010003 and 010004 of the Diego system when their expres-

Table 6. The 901 series: High incidence antigens not assigned to systems or collections

No. Name Symbol Incidence Excluded from Refs % systems

901001 90 1002 Langereis 901003 August 901 005 901006

90 1007 90 1008 901009 Anton

901011 Raph 901012 Sid

90 10 13 Duclos 901014

Vel Lan Ata Jid Ok'

JMH Emm AnWj

MER2 Sd"

PEL

> 99 > 99 > 99 >99 > 99

> 99 > 99 > 99

92 91

>99 >99

1-6, 8,9 1 4 , 6 , 8,9 l 4 , 7 , 9 80 1-6, 8,9, 10 1-4,7,8,9, 12, 13, 17

I , 2,4-6, 8, 81 9, 12, 19

14 ,6 ,8 ,9 , 12, 14, 19

1-9,12,13,15-19

82

Genes controlling 901006 and 90101 1 are located on chromo- somes 19 and 1 1, respectively

27 1

Table 7. Obsolete numbers

Obsolete No. Symbol or previous Current No. Obsolete No. Symbol or previous Current No. symbol symbol

001 005 003002 003003 0040 13 0040 14 0040 15 0040 I 6 004024 004025 00403 8 0050 10 0050 I5 006008 006009 0060 15 0 I600 1 0 16002 0 I6003 0 I6004 02000 1 Collection 201 Collection 202 Collection 203 Collection 204 205003 205004

' See system 16.

H P Pk Rh" Rh' Rh' Rh" E' LW Duclos Singleton Anton K W

KL Kx LW I phenotype LW2 phenotype LW1 phenotype LW4 phenotype Ge 1 GE CROMER IN AU Y k" Kn"

018001 20900 1 209002 Obsolete Obsolete Obsolete Obsolete Obsolete Obsolete ' 901013 Obsolete 90 1009 Obsolete Obsolete 019001 Obsolete Obsolete Obsolete Obsolete Obsolete System 020 system 02 I System 023 005018and005019 022005 02200 1

205005 205006 205007 Collection 206 Collection 2 1 1 70000 1 700007 700009 70001 I 7000 I 2 70001 6 700020 700023 700024 700025 70003 1 700032 700033 700035 700036 700038 700042 700048 90 1004 901010

Knh McC" SIC' GY WR Wr* Ls" Wb Or Gf Heibel An"

R1" (= Ls") In" Dh* POLL 0 s d Tc Tc' Hov (= Wu) WES (WES") FPTT J o" Wrb

Hey

022002 022003 022004 0 14003 and 0 14004 0 10003 and 0 10004 0 10003 020006 020005 00203 1 Obsolete Obsolete 020007 Obsolete 020006 023001 020008 Obsolete 002038 02 I003 02 1004 7000 1 3 02 I008 004050 0 I4005 0 10004

sion was shown to be governed by the same locus as that controlling 010001 (Did) and 010002 (Dib).

J. P. McAlpine, University of Manitoba, Department of Hu- man Genetics, T250-770 Bannatyne Ave., Winnipeg, Man., Canada; fax +1204 786 8712).

Procurement of ISBT Numerical Designations

Choice ojSymbol Symbols for designations of new specificities will con-

sist of 3-6 on-line capital letters and must not duplicate, al- phabetically or phonetically, any current or obsolete sym- bols shown in the tables. Also, symbols used in related fields, such as those used for platelet and leucocyte anti- gens, must be avoided. A list of symbols and names that have been used and are, therefore, no longer suitable for new antigens, are found in Appendix 1 of the 1990 mono- graph [l]. Symbols for specificities that may herald new blood group systems, and thus new genes, have the further constraint that they must differ from any symbols given to genes by the HUGO Nomenclature Committee (Chair: Dr.

Procedures.for Acquisition ofan ISBT Number The initial stipulation is that materials for defining the

new specificity be available for either circulation or in- house testing; the futility of defining a new specificity from which future new specificities cannot be distinguished is obvious. Forms for the entry of required information are ap- pended; they should be photocopied, completed, and for- warded to the appropriate Working Party member as indi- cated below.

For a New Blood Group System or Collection. Proposals with supporting data should be submitted to Dr. G.L. Da- niels; decisions will be based on consensus of the full mem- bership of the Working Party.

For a Specificity Number within an Established System. (1) For a low incidence antigen complete columns A and H

272 ISBT Working Party Blood Group Terminology I995

of Appendix 1 and column C of Appendix 2 for the pertinent blood group system and for the 700 and 901 series; (2) for a high incidence antigen complete column C of Appendix 1 and columns A and B of Appendix 2 for the pertinent blood group system and for the 700 and 901 series; (3) for all anti- gens complete parts A, B, C, and E of Appendix 3, and (4) submit to Prof. Dr. W. Dahr for the MNS system, Dr. P. D. Is- sitt for the Rh system, and Dr. J. Jarrgensen for other sys- tems.

For a Specificity Numher in a Current Collection. (1) For a low incidence antigen complete columns A and B of Ap- pendix 1 and column C of Appendix 2 for the pertinent col- lection and for the 700 and 901 series; (2) for a high inci- dence antigen complete column C of Appendix 1 and co- lumns A and 8 of Appendix 2 for the pertinent collection and for the 700 and 901 series; (3) for all antigens complete parts A, B, D, and E of Appendix 3, and (4) submit forms to Dr. D. J. Anstee or Dr. G. L. Daniels.

Forrr 700 Numbev: (1) Complete columns A and B of Ap- pendix I, the list includes antigens that would qualify as low incidence only in selected populations, e.g. KELl in Orien- tals; (2) completion of column C of Appendix 2 is optional; (3) complete parts A, B, and E of Appendix 3, exclusion of an antigen from a system automatically distinguishes it from low incidence antigens within that system; (4) submit forms to Dr. A. Lubenko who is authorized to assign a 700 number for a new, authenticated specificity.

For u 901 Numbev: (1) Complete columns A and B of Ap- pendix 2; (2) completion of column C of Appendix 1 is op- tional; (3) complete parts A, B, and E of Appendix 3, exclu- sion of an antigen from a system automatically distinguish- es it from high incidence antigens within that system, and (4) submit forms to Dr. G. L. Daniels who is authorized to assign a 901 number for a new, authenticated specificity.

Future Considerations

The 6-digit, genetically based terminology for red cell surface antigens has been in operation for about 10 years now and is generally accepted as a method of classifying and cataloguing blood group specificities. It has been sug- gested that the Working Party should now address other is- sues, such as numbering the red cell determinants detected by cold agglutinins, numbering epitopes of the RH1 (D) an- tigen and other complex specificities, and defining a termi- nology for abnormal phenotypes in complex systems, in particular the MNS system. These issues will be considered by the Working Party in their next meeting in Tokyo in 1996.

Conclusions

Having fulfilled its original brief of devising a uniform nomenclature that is both eye and machine readable and in keeping with the genetic basis of blood groups, the Working Party now functions primarily to monitor and update the ter- minology. In order for the terminology to remain compre- hensive, it is important that all new specificities eligible for inclusion are submitted for procurement of an ISBT number and are provided with a suitable symbol. The Working Party strongly urges that all authors in the field of human red cell blood groups use the terminology provided in tables 2-6 in either the alphabetical/numerical format (e.g. FY2) or the ‘popular’ alternative format (e.g. Fyb). For clarity, it is often advisable when using the more traditional terminology to include the ISBT terminology in parentheses, for example And (GE7).

All members of the Working Party are prepared to handle requests for advice or assistance in any aspect of an investi- gation or to direct them to the most appropriate authority. Addresses and fax numbers of members are provided in Ap- pendix 4. The Chair of the Working Party would be happy to receive any comments or criticisms of the terminology and would raise them at a Working Party meeting. Membership of the Working Party is open to colleagues who wish to par- ticipate actively in deliberations.

Acknowledgements

Since 1990 the following colleagues have retired from the Working Party: Dr. G.WG. Bird; Dr. E. Brodheim; Dr. M. Contreras; Ms M.C. Crookston; Dr. C.P. Engelfriet; Dr. C.M. Giles; Prof. M. Lewis; Dr. W. L. Marsh; Ms J. McCreary; Dr. B. P. L. Moore; Ms P. Morel; Dr. H. Nevanlinna; Dr. R. Nordhagen; Dr. J. Pehta; Dr. R. E. Rosenfield; Dr. P. Rubinstein; Dr. Ch. Salmon; Dr. P. Tippett; Dr. R.H. Walker; Dr. G. Woodfield, and Mr. S. Young. We are extremely grateful for their con- tributions. In particular, we wish to thank Prof. Marion Lewis who chaired the Working Party from 1984 to 1990 and was the primary au- thor ofthe 1990 monograph on which this publication is based.

213

Appendix 1

Applicution for ISBT Number For Low Incidence Antigen. Column A: indicate + or- for result of

testing ‘new’ antibody with cells carrying numbered antigen. Co- lumn B: indicate + or - for result of testing ‘new’ antigen with anti- body specific for numbered antigen.

For High Incidence Antigen. Column C: indicate + or - for results oftesting cells of ‘new’ antibody producer with antibody specific for numbered antigen.

Proposed name ~ - Proposed symbol - Incidence

A B C A B C A B c

RH40 RH42 RH43 RH45 RH48 RH49 RH50 LU 1 LU9 LU14 KELl KEL3 KEL6 KELlO KEL17 KEL2 1 KEL23 KEL24 DI 1 _ _ _ _ ~ D13 YT2 ~-

SC2 C 0 2 LW7 CHIRG7 GE5 GE6 GE7 GE8 _ _ ~ - CROM3 _______.

CROM4 CROM8 KN2 IN 1

ER2

700.2 700.3 -_ - . __ ~~

700.4 700.5

Bgd .

Bgh Bg‘ ~ ~

274 ISBT Working Party Blood Group Terminology I995

Appendix 2

Apylicurion,jor ISBT Number For High Incidence Antigen. Column A: indicate + or ~ for result

of testing ‘new’ antibody with cells negative for numbered specificity. Column B: indicate + or - for result of testing cells of ‘new’ antibody producer with antibody specific for numbered antigen.

For Low Incidence Antigen. Column C: indicate + or - for results oftesting ‘new’ antibody with cells negative for numbered antigen.

~ Proposed symbol Incidence Proposed name

A B C

RH17 RH18 RH29 RH34 RH44 RH46 RH47 RH5 1 LU2 LU3 LU4 LU5 LU6 LU7 LU8 L u l l LU12 LU13 LU16 LU17 LU20 KEL2 KEL4 KELS KEL7 KELl1 KEL 12 KEL 13 KEL 14 KEL 16 KELlX KEL19 KEL20 KEL22

A B C A B C

FY3 FY5 JK3 D12 D14 YTl sc 1 sc3 DO3 DO4 DO5 co 1 C 0 3 LW5 LW6 CHIRG 1 CHIRG2 CHIRG3 CHIRG4 CHIRGS CHIRG6 CH/RG I 1 CHIRG 12 HI XK 1 GE2 GE3 GE4 CROM 1 CROM2 CROMS CROM6 CROM7 CROM9 CROM 10 KN 1 KN3 KN4 KN 5 IN2

COST 1 11 12 ER2 GLOBO 1 GLOBO 3

901.1 901.2 901.3 901.5 901.6 901.7 901.8 901.9 901.1 1 901.12 901.13 901.14

275

Appendix 3 Appendix 4

Application,fi,r an ISBT Number

Proposed name Proposed symbol

Ai Inheritance: ratio +:-offspring ~ _ _ _ Aii inheritance: ratio +:-siblings ~

B Exclusion from blood group systems: List systems and z counts' for each List substitute markers and z counts for each

C' Inclusion in a system: system name ~

Genetic: give lods at 0 = 0.00' Serological: give details (e.g. altered expression of other antigens in system) Biochemical:

D Inclusion in a collection: collection name Genetic: Serological: Biochemical:

E Pertinent serum available for: in-house testing , circulation Pertinent cells available for: in-house testing , circulation

Investigator: Date

For a 700 number complete parts Ai, B, and E; for a 901 number complete parts Aii, B, and E; for inclusion in a system complete parts A, B, C, and E; for inclusion in a collection complete parts A, B, D, and E. ' Consult Race and Sanger [83] for determination.

Addresses and Fax Numbers of Working Party Menzhers Dr. D. J. Anstee: International Blood Group Reference Laboratory,

Southmead Road, Bristol BS 10 5ND (UK). Fax +44 272 59 1 660 Dr. J. P Cartron: INTS, 6, rue Alexandre-Cabanel, F-75739 Paris Cc-

dex 15 (France). Fax +33 1 47 34 74 3 1 Prof. Dr. W. Dahr: Scientific Consultation and Translations, Graf-Her-

mann-Strasse 15, D-5 1429 Bergisch Gladbach (Germany). Fax +49 2204 55989

Dr. G. L. Daniels: Blood Group Unit, Bristol Institute of Transfusion Science, Southmead Road, Bristol BS 10 5ND (UK). Fax +44 1 179 591 660

Dr. P. D. Issitt: Transfusion Service, Duke University Medical Center, PO Box 2928, Durham NC 27710 (USA). Fax +1919 68 I 8969

Dr. J. Jerrgensen: Regional Blood Transfusion Center, Department of Clinical Immunology, University Hospital, Skejby, DK-8200 Kr- hus N (Denmark). Fax +45 8949 6007

Dr. L. Kornstad: Statens institute for Folkeshelse, Department of Im- munology, National Blood Group Reference Laboratory. Cicit- myrsveien 75, N-0462 Oslo 4 (Norway). Fax +47 2 2353605

Dr. C. Levene: Reference Laboratory for lmmunohaematology and Blood Groups, National Blood Services Centre, Magen David Adom, Tel Hashomer 52621 (Israel). Fax +972 238 2256

Ms. C. Lomas-Francis: 3220 Duval Road, Apt 1205, Austin, TX 78759 (USA)

Dr. A. Lubenko: Yorkshire Blood Transfusion Service, Bridle Path, Leeds LSI 5 7TW (UK). Fax +44 113 2603925

Ms. D. Mallory: National Reference Laboratory for Blood Group Sc- rology, American Red Cross, 15601 Crabbs Branch Way, Rock- ville, MD 20855-2743 (USA). Fax + I 301 738 0666

Mr. J. J. Moulds: Gamma Biologicals Inc., 3700 Mangum Road, Houston, TX 77092 (USA). Fax + I 713 956 3333

Dr. Y. Okubo: Osaka Red Cross Blood Center, 4-34 Morinomiya, 2- Chome, Joto-Ku, Osaka 536 (Japan). Fax +81 6 968 4900

Dr. M. A. M. Overbeeke: Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, PO Box 91 90, Amsterdam (The Netherlands). Fax +3 I 20 5 12 3332 or +3 1 20 5 12 3474

Dr. M. E. Reid: New York Blood Center, 3 10 East 67th Street, New York,NY 10021 (USA). Fax+1 2127374935

Dr. Ph. Rouger: Centre national de Reference pour les Groupes san- guines, CNTS St Antoine, 53, boulevard Diderot, F-75571 Paris Cedex 13 (France). Fax +33 1 43 06 04 83

Prof. Dr. S. Seidl: Blutspendedienst Hessen, Sandhofstrasse I , PB 730367, D-6000 Frankfurt a.M. 71 (Germany). Fax +49 69 678 21 10

Dr. P Sistonen: Finnish Red Cross Blood Transfusion Service, Kivi- haantie 7, SF-003 10, Helsinki 31 (Finland). Fax +358 0 5801 329

Dr. S. Wendel: Blood Bank, Hospital Sirio-Libanes, Rua Dona Adnia Jafet 91,29 Andar, SHo Paulo (Brazil). Fax +55 I 1 257 1290

Dr. T. Zelinski: Rh Laboratory, 735 Notre Dame Avenue, Winnipeg, Man. R3E OL8 (Canada). Fax + I 204 787 4807

276 ISBT Working Party Blood Group Terminology 1995

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18 Chaudhuri A, Polyakova J, Zbrzezna L: Wil- liams K, Gulati S , Pogo AO: Cloning of glyco- protein D cDNA, which encodes the major sub- unit of the Duffy blood group system and the receptor for the Plasmodium vivax malaria par- asite. Proc Natl Acad Sci USA 1993;90:10793- 10797.

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24 Zelinski T, Coghlan G, White L, Philipps S : The Dicgo blood group locus is located on chromo- some 17q. Cienomics 1993;17:665-666.

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26 Bruce LJ, Ring SM, Anstee DJ, Reid ME, Wil- kinson S, Tanner MJA: Changes in the blood group Wright antigens are associated with a mu- tation at amino acid 658 in human erythrocyte band 3: A site of interaction between band 3 and glycophorin A under certain conditions. Blood 1995;85:541-547.

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28 Spring FA, Gardner B, Anstee DJ: Evidence that the antigens of the YT blood group system are located on human erythrocyte acetylcholin- esterase. Blood I992;80:2136-2 141.

29 Bartels CF, Zelinski T, Lockridge 0: Mutation at codon 322 in the human acetylcholinesterase (ACHE) gene accounts for YT blood group po- lymorphism. Am J Hum Genet 1993;52:928- 936.

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40 Shows TB, McAlpine PJ, Boucheix C, Collins FS, Conneally CM, Frezal J, Gershowitz H, Goodfellow PN, Hall JG, lssitt P, Jones CA, Knowles BB, Lewis M, McKusick VA, Meisler M, Morton NE, Rubinstein P, Schanfield MS, Schmickel RD, Skolnick MH, Spence MA, Sutherland GR, Traver M, Van Cong N, Willard HF: Guidelines for human gene nomenclature. An international system for human gene no- menclature (ISGN, 1987). Cytogenet Cell Ge- net 1987;46: 11-28,

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42 Skov F, Green C, Daniels G, Khalid G, Tippett P: Miltenberger classlX of the MNS blood group system. Vox Sang 1991;61:130-136.

43 Huang C-H, Skov F, Daniels G, Tippett P, Blu- menfeld 00: Molecular analysis of human gly- cophorin MilX gene shows a silent segment transfer and untemplated mutation resulting from gene conversion via sequence repeats.

44 Rcid ME, Moore BPL, Poole J, Parker NJ, Asenbryl E, Vengelen-Tyler V, Lubenko A, Gal- ligan B: TSEN: A novel MNS-related blood group antigen. Vox Sang 1992;63: 122-128.

45 Reid ME, Poole J, Green C, Neil1 G, Banks J: MINY: A novel MNS-related blood group anti- gen. Vox Sang 1992;63:129-132.

46 Tippett P, Rcid ME, Poole J, Green CA, Daniels GL, Anstee DJ: The Miltenberger subsystem: Is it obsolescent'? Transfusion Med Rev 1992;6:

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48 Daniels GL, Green CA, Okubo Y, Seno T, Ya- maguchi H, Ota S, Taguchi T, Tomonari Y: SAT, a 'new' low frequency blood group antigen which may be associated with two different MNS variants. Transfusion Med 1991;1:3945.

49 Huang C-H, Reid ME, Okubo Y, Daniels GL, Blumenfeld 00: Glycophorin SAT of the hu- man erythrocyte membrane is specified by a hy- brid gene reciprocal to glycophorin Dantu gene.

50 Uchikawa M, Tsuneyama H, Wang L, Tokunaga K, Juji T, Tadokoro K, Enomoto T A novel ami- no acid sequence result in the expression of the MNS related private antigen. SAT (abstract). Vox Sang 1994;67(suppl2):116.

5 I Daniels GL, Green CA, Poole J, Jerne D, Smart E, Wilcox D, Young S: ERIK, a low frequency red cell antigen ofthe MNS blood group system associated with St". Transfusion Med 1993;3:

52 Huang C-H, Reid M, Daniels G, Blumenfeld 00: Alteration of splice site selection by an ex- on mutation in the human glycophorin A gene. J Biol Chem 1993;268:25902-25908.

53 Huang C-H. Reid M, Daniels G, Blumenfeld 00: Gene conversion between glycophorins A and E results in Std glycophorin in a family ex- hibiting the Erik/StJ blood group phenotype (abstract). Blood 1994;84(suppl 1):238a.

54 Daniels GL, Green CA, Petty AC, Green F, Okubo Y The low frequency antigen 0s" is lo- cated on glycophorin A (abstract). Transfusion Med 1993;3(suppl 1):85.

55 Marais 1, Moores P, Smart E, Martell R: STEM, a new low-frequency Rh antigen associated with the e-variant phenotypes hrs- (Rh:-18,- 19) and hr"- (Rh:-3 1,-34). Transfusion Med 1993;3:354 I .

56 Bizot M, Lomas C, Rubio F, Tippett P: An anti- serum identifying a red cell determinant ex- pressed by Rh:33 and by some 'new' depressed Rh phenotypes. Transfusion 1988;28:342-345.

57 Lomas C, Grassmann W, Ford D, Watt J, Gooch A, Jones J, Beolet M, Stern D, Wallace M. Tip- pett P: FPTT is a low-incidence Rh antigen as- sociated with a 'new' partial Rh D phenotype, DFR. Transfusion 1994;34:612-616.

58 Sistonen P, Sareneva H, Pirkola A, Eklund J: MAR, a novel high-incidence Rh antigen re- vealing the existence of an allelic sub-system including C" (Rh8) and C" (Rh9) with excep- tional distribution in the Finnish population. Vox Sang 1994;66:287-292.

59 Daniels GL: Evidence that the Auberger blood group antigens are located on the Lutheran gly- coproteins. Vox Sang 1990;58:56-60.

60 Zelinski T, Kaita H, Johnson K, Moulds M: Ge- netic evidence that the gene controlling Auh is located on chromosome 19. Vox Sang 1090;58: 126-1 28.

61 Zelinski T, Kaita H, Coghlan G, Philipps S: As- signment of the Auberger red cell antigen poly- morphism to the Lutheran blood group system: Genetic justification. Vox Sang 1991;61:275- 276.

Blood 1995;85:2222-2227.

129-1 35.

62 Daniels GL, Le Pennec PY, Rouger P, Salmon C, Tippett P: The red cell antigens Au" and Au" belong to the Lutheran system. Vox Sang 1991;

63 Levene C, Gekker K, Poole J, Goldfarb A, Da- Costa Y, Manny N: Lu20, a new high incidencc 'para'-Lu antigen in the Lutheran blood system (abstract). Rev Paul Med 1992; I I 0( suppl I ): 13.

64 Banks JA, Parker N, Poole J: Evidence to show that Dombrock (Do) antigens reside on the Gy'V Hy glycoprotein (abstract). Transfusion Med 1992;2(suppl 1 ):68.

65 Spring FA, Reid ME, Nicholson G: Evidcncc for expression of the Jo" blood group antigen on the Gy'/Hy-active glycoprotein. Vox Sang

66 Zelinski T, Kaita H, Lewis M, Coghlan ( i , White L, Cartron J-P: Distinction of the glyco- phorin C locus from the Diego, Dombrock and Yt blood group loci. Vox Sang 199 I ;6 I :62 64.

67 Daniels G, King M-J, Avent ND, Khalid ( i3 Reid M, Mallinson G, Smythe J, Cedergren L3: A point mutation in the GYPC gene results 111

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68 King MJ, Avent ND, Mallinson G, Reid ME: Point mutation in the glycophorinC gene re- sults in the expression of the blood group anti- gen Dh'. Vox Sang 1992;63:56-58.

69 Lewis M, Kaita H, Philipps S, McAlpine PJ, Wong P: Exclusion of unassigned blood group system loci from the regulator of complement activation gene cluster on chromosome I q32. Vox Sang 1989;57:210-212.

70 Moulds JM, Moulds JJ, Brown M, Atkinson JP: Antiglobulin testing for CR 1 -related (Knops: McCoy/Swain-LangleylYork) blood group anti- gens: Negative and weak reactions arc caused by variable expression of CR1. Vox Sang 1992;

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73 Rouse D, Weiner C, Williamson R: Immune hy- drops fetalis attributable to anti-HJK. Ohstct Gynecol 1990;76:988-990.

74 Hoffman JJML, Overbeeke MAM, Kaita ti, Loomans AAH: A new, low-incidence red ccll antigen (HOFM), associated with depressed ( ' antigen. Vox Sang 1990;59:240-243.

75 Coghlan G, Green C. Lubenko A, Tippett P, Ze- linski T Low-incidence red cell antigen EL.0 (700.5 1): Evidence for exclusion of thirteen blood group systems. Vox Sang 1993;64:240 243.

76 Stem DA, Hawksworth DN, Watt JM, Ford 11s: A new low-frequency red cell antigen 'SA- RAH'. Vox Sang 1994;67:64-67.

77 Coghlan G, McCreary J, Underwood V, Zelin- ski T: A 'new' low-incidence red cell antigen, LOCR, associated with altered expression of Rh antigens. Transfusion I994;34:492495.

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78 Hamilton JR, Coghlan G: Unpublished obser- vationa, 1993.

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82 Daniels GL, Simard H, Goldman M, Taliano V, Fleury M, Spurll G, Garcia C, Ouellet P, Decary F: PEL, a new high frequency red cell antigen (abstract). Transfusion I994;34(suppl):26S.

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