blood group terminology 1990 - isbt: international … cells/reports... · vox sang....

Vox Sang. 1990;58:152-169

Blood Group Terminology N901 From the ISBT Working Party on Terminology for Red Cell Surface Antigens

Section Editors: M . Garretta, Les Ulis

C. E Hogman, Uppsala

M . Lewis (Chairman), D. J . Anstee, G. W. G. Bird, E. Brodheim, J.-P. Cartron, M . Contreras, M . C. Crookston, W. DahP; G. L. Daniels, C. P. Engelfriet, C. M. Giles, P. D. Issitt, J . J@rgensen, L. Kornstad, A. Lubenko, W. L. Marsh, J. McCreary, B. P. L. Moore, f? Morel, J. J. MouIds, H. Nevanlinna, R. Nordhagen, I: Okubo, R. E. Rosenfield, Ph. Rouger, P. Rubinstein, Ch. Salmon, S. Seidl, P. Sistonen, P. Tippett, R . H. Walker, G. Woodfield, S. Young

The formation of an ISBT Working Party on Terminol- ogy for Red Cell Surface Antigens was initiated by Dr. B. P. L. Moore on the recommendation of the ISBT Work- ing Party on Automation and Data Processing. The man- date was to establish a uniform nomenclature that is ‘both eye and machine readable, and in keeping with the genetic basis of blood groups’. The inaugural meeting, under the chairmanship of Dr. F. H. Allen, Jr., occurred in Montreal on August 16th, 1980, at the 16th Congress of the ISBT. The fundamental feature adopted was a six-digit identification number for each of the authenticated blood group specificities, for computer use. Further, these numbers would be suitably ordered for adaptation to a combined alphabeticall numerical system, based on the model devised for the Rh blood group system [1], for general use. There was unani- mous agreement that existing terminology would not be altered, but that designations for genes/loci, for the al- phabeticahumerical system, and for new specificities would be restricted to on-line capital letters of the Latin alphabet and Arabic numerals.

Subcommittees were created to work out details that were discussed at subsequent meetings chaired by Dr. Al- len (New York, October 29th, 1981; Budapest, August lst, 1982) and by Prof. M. Lewis (Munich, July 21st, 1984), and that were the subjects of reports [2-4] . Further specificities given numerical designations at the Sydney meeting on May llth, 1986 (Acting Chairman, Dr. M. Contreras) have also been the topic of a publication [ 5 ] . At the most recent meeting of the Working Party members (London, July loth,

’ This monograph is dedicated to the memory of the late Dr. E H. Al- len, Jr., whose leading role in the efforts of the Working Party cannot be overemphasized.

1988; Chairman, Prof. Lewis), the decision was taken to prepare this monograph as a comprehensive statement doc- umenting guidelines, rationale, and the current state of affairs. Throughout, references given in the tables for descriptions of specificities are restricted to post-1974 publications (for earlier references see Race and Sanger [6]) and are not repeated in the text. Consequently, in many in- stances, statements made in the text are not validated therein, but can be verified by perusal of the tabulated publications. Furthermore, the citations are limited to those which qualify a specificity for a number; for a complete bibliography up to 1985, the reader should consult Issitt [7] .

Blood Group Systems

Historical Concepts. Prior to the recent advances in gene mapping and in the biochemical characterization of antigens, proof of control by a single gene was based on classical family studies and population statistics demonstrating an antithetical relationship between a pair of antigens, e.g. M and N. An indication of the likelihood of allelic relationships, based on the initial failure to observe disruption of the parental allele alignment in at least one of two or more sibs, i.e. failure to detect recombination between the genes, coupled with evidence of linkage disequilibrium, was acceptable for inclusion within a blood group system, e.g. MN and Ss. Further, specificities were placed within systems when the defining antibody failed to react with pertinent ‘null type’ red cells, i.e. the expansion of the Lutheran system to include a number of high-incidence specificities. Also, antigens produced in the same biosyn-

153 ISBT/ICSH Working Party

Table 1. Designations for blood group systems and antigen specificities

Name Symbol No. No. within system

001 002 003 004 005 006 007 008 009 010 011 012 013 014 015 016 017

ABO ABO 001 A B A,B A1 .., MNS MNS 002 M N S s U He Mi" M Vw Mur Me V' Me Mta St" Ria Cl' P P1 003 P1 . . . . . . Rh RH 004 D C E c e f Ce Cw Cx V EW G RhA RhB RhC RhD Hr,, Lutheran LU 005 Lu" Lub Luab Lu4* LuS* Lu6* Lu7* Lug* Mull ... Lull*Much Hughes Lu14* ... Lu16 Lui7* Kell KEL 006 K k Kp" Kpb KU Js" Jsb . . . . . . U1" Cote BBc' K13* Sans ... 'k-like' Wka Lewis LE 007 Lea Leb Leab Duffy FY 008 Fya Fyb Fy3 Fy4 Fy' Fy6 Kidd JK 009 Jk" Jkb Jkab Diego DI 010 Dia Dib Yt YT 011 Yt" Ytb xg XG 012 Xga Scianna SC 013 Sm Bu" SC' Domhrock DO 014 Do" Dob Colton CO 015 Coa Cob Coab Landsteiner-Wiener LW 016 . . . . . . . . . . . . LWa LWab LWb Chido/Rodgers CWRG 017 Chl Ch2 Ch3 Ch4 ChS Ch6 WH Rgl Rg2 Hh H 018 H Kx XK 019 Kx

Referenced descriptions of all of the specificities may be found in Race and Sanger [6] excepting for LU13 (not the subject of a report;7p620), LU14 [Transfusion (Phila) 1975;15:523], LU16 [Transfusion (Phila) 1980;20:630], LU17 [Can J Med Tech 1979;41:43], FY6 [J Exp Med 1987;166:776], and for those in systems 16 and 17 (see text).

system or to a collection. For the record, they were initially used as follows: AB05 for H, P12 for P, P13 for Pk, LUlO for Singleton, LU15 for Anton, KELS for Kw, KEL9 for KL, KEL1S for Kx, and LW1, 2 , 3 & 4 for phenotype designations. *

... indicates that a number is now obsolete, the specificity having been removed altogether because of inadequate documentation or to another

In our earlier publications [3, 41 full names were used; here we revert to the designations as originally published.

thetic pathway have been ascribed to a system, e.g. A, B, and H. Finally, single antigens shown to be controlled by genes other than those of already described systems, initiated a new system, e.g. Yt". Definition of a new system resulted from classical family studies in which the gene of a new system was proven to assort independently of the genes of the old, i.e. recombination was observed.

Current State. The present composition of the blood group systems is set out in tables 1 and 2. The six-digit computer numbers have been devised so that the first three numbers represent the system, and the remaining three the specificity: 001001 represents the A specificity in the ABO system. The alphabetical names of the systems and their constituents have not wittingly been altered from those of the initial descriptions; the symbol for use as genellocus designation and as the alphabetical component of the al- phabeticalhumerical system has been converted to capital letters. This device provides an alternative nomenclature that allows uniformity and conforms to the regulations of

the Human Gene Mapping Nomenclature Committee (HGMNC) [8]. For textual and verbal use, sinistral zeros in system and specificity designations may be omitted. Thus, to date, the established systems number 1 to 19, and the Rh specificities, for example, number RH1 to RH48 (note, there is no space between the symbol and the number).

Systems 1-15 have longstanding tenure [6]; antithetical relationships (low: high incidence) not readily discernible by symbol have been proposed for LU9: LU6, LU14:LU8, KEL17 : KELll and KEL24: KEL14. It should be under- stood that system 7 refers to serologically defined products of the LE gene, not to secretor status. Much-used alternative names for some specificities may be found in Issitt [7].

System 16. The discovery of the LWb antigen (originally called Nea [9]), recognition of its antithetical relationship to LWa [lo], and distinction of its locus from the loci for systems 1-15 [ll], justify system status for LW.

SystemIZ The CH/RG antigens are carried on the fourth component of complement. C4A and C4B are contiguous

flegelwa

Rectangle

flegelwa

Rectangle


Table 2. Extension of blood group system specificities

No. System Reference System Reference System Reference within symbol symbol symbol system System No. System No. System No.

018 019 020 021 022

023

024

02s 026 027 028 029

030

03 1 032

033 034 035 036 037 038 039

040

04 1

042

043

044

045

046

047

048

MNS 002 NY" Hut Hi1 MV Far

SD

Mit

Dantu

Nob Ena En"KT

"

Or

HOP

Vox Sang 1977;32:269.

Transfusion (Phila) 1981;21:614. Vox Sang 1980;39:331

Vox Sang 1984;46:377. Vox Sang 1982;42:256. Vox Sang 1982;42:256.

Transfusion (Phila) 1985;25:51. J Immunogenet 1975;2:87. Vox Sang 1987;52:330.

RH 004 Hr hrs vs CG CE

DW

ET

... e-like cE hrH 'total Rh'

Goa

hrB Rh32

Har HrB* Rh35* Be" Evans

Rh39

Tar

Rh41

Cces*

Crawford

Nou

Riv

Sec

Dav

JAL

...

KEL 006 K18* Sub* Km

K22*

K23 *

CIS

KP'

Transfusion (Phila) 1989; 19:798

Vox Sang 1978;34:208.

Transfusion (Phila) 1979; 19: 389. Am J Hum Genet 1979;31:630. Transfusion (Phila) 1981;21:150. Transfusion (Phila) 1980;20:631. Transfusion (Phila) 1980;20:631. Blood Transfus Immunohae- matol 1981;24:117. Transfusion (Phila) 1983;23:410. Transfusion (Phila) 1989;29:798. Blood Transfus Immunohae- matol1982;25:18S. Poole J et al: personal commun.

Vox Sang 1975:29:124 Vox Sang 1979;36:97. Vox Sang 1979:36:375. Vox Sang 1979;36:29. Transfusion (Phila) 1981;21:613. Transfusion (Phila) 1985;25:471. Transfusion (Phila) 1985;25:448

Descriptions of specificities not referenced will be found in Race and Sanger [6]. . . . indicates obsolete numbers; for the record they were initially used as follows: RH25 for LW, RH38 for Duclos. In our earlier publications [3,4] other names were used; here we revert to the names of the initial publications or recommendations of the author. *

ISBTIICSH Working Party 155

Table 3. Sample phenotype and genotype designations

System Traditional Alternative

Colton Phenotype Co(a+b-) co:1,-2

coalco" co I l l

CO"lC0 co 110

Phenotype Co(a+b+) c0:1,2

Genotype or or

Genotype Co"lCoh co 112

Phenotype Co(a-b+) c0:-1,2

Genotype C o ~ l C o ~ or COhlCO

co 212 or co 210

~ ~~

Phenotype Co(a-b-ab-) c0:-1, -2, -3

Genotype COlCO co 010

Kell Phenotype K- k f Kp(a-b+) Js(a-b+) KEL: -1,2,-3,4,-6,7

Genotype k, Kph, Js'lk, Kpb, Jsh or k, Kpb, Js'ftV

K E L 2,4,712,4,7 or KEL 2,4,7/0

and result from gene duplication; their homology is such that RG and CH epitopes, though strongly associated with C4A and C4B, respectively, are not restricted to either isotype. The specificities that form the system have been described in detail: Chl, Ch2, Ch3, Rgl, Rg2 [12]; Ch4, Ch5, Ch6 [13]; WH [14].

System 18. The occurrence of two phenotypes indicates genetic variation in the expression of the ABO precursor gene; the serology, genetics and biochemistry of the Hh system are described in detail by Salmon et al. [15, chapt. 91.

System 19. The occurrence of the rare phenotype Kx-, sometimes due to gene deletion [16, 171, has been docu- mented on many occasions; the Kx protein has recently been isolated [18].

For phenotype designations in the alphabeticallnumerical terminology, the symbol is followed by a colon and then the specificity numbers separated by commas, a negative result being indicated by a preceding minus sign; the phenotype D+ C+ E- c+ e+ or DCce or Rlr would be rendered RH:1,2,-3,4,5. In allele or haplotype designa-

tions, the symbols are italicized, followed by a space or asterisk, and then the numbers, separated by commas, of the defining specificities; CDe or R' becomes RH 1,2,5 and cde or r becomes RH 4 3 . As in current practice, data on non-informative specificities should be included in the text, or a footnote, of publications: e.g. 'all samples were C"-, C-, E"-, Hr+' would be converted to 'all samples were RH:-8, -9,-llJ8'. When a blood group system is defined by a single specificity, traditional designations are converted as follows: Xg(a+) to XG:1, Xg(a-) to XG:-1, Xg' to XGl, and Xg to XG 0, the last conversion making a visual distinction between the gene/locus and the unexpressed allele. Other examples of traditional designations along with their alphabeticallnumerical counterparts are set out in table 3.

Future Considerations. In view of the plethora of blood group antigens already

described, there is reason to speculate that many may signal new blood group systems. Ideally, a system will be composed of antigens whose production is governed by the


Table 4. Chromosomal locations of blood group system genes

Chromosome Arm Locus, region

1 1 4 6 9

18 19 19 22 X 9

RH, lp36-p34 [Sci 1974;183:966]; SC, lp34-p32 [Can J Genet Cytol 1977;19:695] m, lq22-q23 [Proc Natl Acad Sci 1968;61:949] MNS, 4q28-q31 [Ann Hum Genet 1981;45:39] CHIRG, 6~21.3 [Tiss Antigens 1974;4.366; 1976;8:143] ABQ, 9q34 [Ann Hum Genet 1977;41:53] JK, 18qll-ql2 [Hum Genet 1987;77:205] LE, 19p [HGM1,183,1973]; LW 19~13-pll [Ann Hum Genet 1984;48:239] H, 19q [Am J Hum Genet 1981;33:421; LU, 19q12-ql3 [Clin Genet 1983;24:159] PI, 22qll-qter [Cytogenet Cell Genet 1978;22:629] XG, Xp22.3 [Lancet 1962;i:8]; XK, Xp21.1 [Cytogenet Cell Genet 1978;22:531] KEL, DI, YT, DO, CO. There is evidence for linkage between K E L and YT [Vox Sang 1989:57:88]

Chromosomal localizations of genesfloci are identified by the arm (p = short, q = long), followed by the region, and then by the band within the

The first indications of a chromosomal assignment are referenced; for refinements consult the pertinent Committee Report in Human Gene region, in both cases numbered from the centromere. ter = end.

Mapping 9 (Paris Conference, 1987). [Cytogenet Cell Genet 1987;46:102-3151; or references in table 9 of this article.

alleles of a single gene. If all resources are used, exclusion from the established systems of an antigen that is controlled by a ‘polymorphic’ gene (at least one allele having an incidence of >1% ~ 9 9 % ) is feasible unless the locus is contiguous, or very closely linked, to one of those loci involved with the systems. However, when genes are contiguous and share homology (i.e. have a common ancestor) to the ex- tent that hybrid products occur, e.g. M N and Ss, there seems to be no particular advantage to the creation of separate blood group systems. Exclusion of a specificity controlled by a usually ‘non-polymorphic’ gene (allele incidence <1% or >99% in all but selected populations) poses a formidable but, as attested by the proven individuality of systems 10,13 and 16, not insurmountable obstacle.

The chromosomal assignment of 14 of the 19 blood group system loci (table 4) facilitates the elucidation of new systems. The assignments have been achieved by using many sources of information. RH was assigned to chromosome 1 by the loss of an allele product concurrent with a somatic, chromosome segment deletion, and XG to the X chromosome by the pattern of inheritance and the differ- ence in Xg” phenotype frequencies in males and females. Some assignments were made through linkage with other genetic markers in blood: e.g. FY with a cytogenetic polymorphism of centromeric heterochromatin (lqh), CHIRG with a white cell antigen polymorphism (HLA), LE with a plasma protein polymorphism (C3), and JK with a DNA segment defined by a restriction fragment length polymorphism (D18S6).

Guidelines for the establishment of new blood group systems: (1) An antigen whose production is governed by a ‘poly-

morphic’ gene that is distinct from the genes involved in the established systems.

(2)An antigen whose production is governed by a usually ‘non-polymorphic’ gene that is distinct from the genes involved in the established systems and that has a chromosomal assignment. Diego is the only established blood group system that

does not meet the above criteria; its gene does not have a chromosomal assignment. As a consequence, distinction from the Diego system presents the major challenge in the formation of new systems.

Guidelines for the inclusion of a new specificity in an established system: (1) An antithetical relationship between a new antigen and

one already assigned to a system. (2)Evidence, from a linkage analysis of family data, that

the controlling allele is probably a newly recognized form of the pertinent gene, and supporting serological or biochemical data.

Other AntigenslSpecificities

There remain many other specificities that have not been assigned to either established or new systems because

ISBTLCSH Working Party 157

of inadequate data that range from almost nil to sufficient for exclusion from all but one system. Initially we classified these specificities into two series according to incidence: the 700 series for low incidence, and the 900 series for high incidence [4]. However, on further deliberation, we have decided that there is some merit in gathering together, into ‘Collections’, specificities that have a serological, biochemical or genetic connection: these Collections are set out in table 5. A serological connection may be based on dosage results supporting the genetic interpretation, on altered expression of some, or all, of the antigens in certain phenotypes, or on antigen absence in apparent ‘null’ phenotypes. A biochemical connection would be based on studies of the epitope structures, and a genetic connection would be indicated by family and population studies. For textual and verbal communications, sinistral specificity zeros may be replaced by a silent period: e.g. the 201 Collection runs from 201.2 to 201.6.

The Collections 201. These specificities are carried on, or associated

with, glycophorins C andlor D [19,20]; there is no antithetical relationship between the high- and low-incidence specificities. The localization of the GYPC gene to chromosome 2q14-q21 [21] distinguishes it from all but the unassigned blood group system genes: KEL, DI, YT, DO and CO (table4). Classical family studies have excluded Ge from the Kell system [6, p. 4191 and Lsa from the Kell and Colton systems [22].

202. The epitopes designated as having a biochemical connection are carried on a glycoprotein that has a molecular weight of 70 kD [23]. They have been further charac- terized as antigens on the decay-accelerating factor of complement [24], whose locus (DAF) has been linked to the regulator of complement activation gene cluster (RCA) on chromosome lq32 [25]. Failure of the defining antibody to react with IFC- red cells (the Inab phenotype) provides the serological connection [26]. The indicated genetic connections are based on probable antithetical relationships im- plied by the symbols; these have not been substantiated by population statistics indicating Hardy-Weinberg expecta- tion or by Mendelian ratios of offspring phenotypes in the various mating types, but the incidence of Tcb in the Tc(a-) phenotype in Blacks and dosage results in studies of WES do provide support for the interpretation.

The chromosomal localization of DAF distinguishes it from all but the unassigned blood group system genes. If the assumption is made that the Cromer antigens are co- trolled by the DAF gene as well as being carried on its protein, classical family studies with 202.8 (WES”) as the

critical marker allow exclusion of the Cromer antigens from the Kell, Dombrock and Colton systems. Finally, non-linkage of the unassigned loci with F13B [27], a member of the closely linked RCA gene cluster, establishes the singularity of DAF relative to systems 1-19.

203. Both epitopes are carried on the CD44 glycoprotein (MW 80 kD) [28] whose gene has been localized to chromosome 11~13; In” bears an antithetical relationship to Inh. System status requires distinction of IN from the unassigned blood group system loci.

204. The two Auberger specificities bear an antithetical relationship. The antigens have been excluded, by classical family studies, from all established systems except Diego [29,30]. Simultaneous, independent genetic and biochemical studies assigning the gene controlling Aub production to chromosome 19q12-ql3 [31] and demonstrating that the Auberger antigens are carried on the Lutheran glycoproteins [32], suggest an integral relationship between the Au- berger and Lutheran epitopes.

205. These specificities are gathered together because a disproportionate number of red cell samples lack all of the high-incidence members. The antithetical relationship of 205.1 & 2 has been substantiated by population studies whereas that of 205.4 & 5 has not. Family data indicate that 205.1,2 & 3 are under different genetic control than are 205.4,5 & 6 [33].

206. The disproportionate number of red cell samples from Caucasians that lack both specificities provides the serological connection [34].

202 For a detailed account of studies on I and i, the reader is referred to Salmon et al. [15, chapt. 121; virtually all red cell samples carry some i.

208. The Er antigens appear to bear an antithetical relationship; a silent allele is postulated to account for the four observed phenotypes. Erb has not been distinguished from all other ISBT-numered low-incidence antigens.

209. These antigens have been studied for a long time but the exact nature of their relationship to each other and to P1 remains unresolved [15, chapt. 131. Although P1, Pk and P derive from a common precursor (ceramide dihexo- side), they are produced in different pathways. Pk is the biochemical precursor of P (globoside) and LKE is thought to be synthesized in this pathway rather than in that of P1 (paragloboside). The syntenic assignment of P to chromosome 6 [35] has yet to be confirmed.

As a result of the formation of Collections, the 700 Series is only slightly affected, but the 900 Series was much depleted and is replaced by the 901 Series. As with the Collections, sinistral specificity zeros may be replaced with a silent period for textual and verbal communications.

158 ISBTDCSH Working Party

Table 5. Collections of antigenshpecificities with serological, biochemical or genetic connections

Collection Specificity Connection Reference

No. name symbol No. symbol inci- sero- biochem- genetic dence % logical ical

201 Gerbich GE 201002 Ge2 >99 X X

201003 Ge3 >99 X X

201004 Ge4 >99 X X

201005 Wb <1 X

201006 Ls" <I X

Biochem J 1984;221:97 Hoppe Seyler Biol Chem 1987;368:1375 Br J Haematol 1988;70:477 Biochem J 1985;232:289; Vox Sang 1986;50:112 Abst M ISBT p 156, 1988

202 Cromer CROMER 202001 Cra 202002 Tc" 202003 Tcb 202004 Tcc 202005 Dra 202006 Esa 202007 IFC 202008 WES" 202009 WESb 202010 UMC

>99 299 <1 <1 >99 >99 >99 <1 >99 >99

X X

X X

X X X

X X

X

X X

X X

Transfusion (Phila) 1975;15:522 Transfusion (Phila) 1983;23: 124

X Transfusion (Phila) 1982;22:413; 1985;25:373 X Transfusion (Phila) 1982;22:413

Transfusion (Phila) 1984;24: 13; 1987;27:64 Abst XVIII ISBT p 163, 1984 Transfusion (Phila) 1988;28:427

X Vox Sang 1987;52:111 Vox Sang 1987;53:235 Transfusion (Phila) 1989;29:794

~~

203 Indian IN 203001 Ina <1 X X Vox Sang 1974;26;400 203002 Inb >99 X X Vox Sang 1975;29:73

-__-

204 Auberger AU 204001 Au" 90 X Vox Sang 1982;43:259 204002 Aub 50 X Vox Sang 1989;56:54

~ _ _ - 205 Cost COST 205001 Cs" 95 X

205002 Csb 34 205003 Yk" 95 X 205004 Kn" >99 X

205005 Knb 5 205006 McCa >99 X

205007 SI" 99 X

Am J Med Tech 1983;49:49

Vox Sang 1975;29:145 X Med Lab Sci 1987;44:94

x Transfusion (Phila) 1980;20:630 Transfusion (Phila) 1978;18:566 Transfusion (Phila) 1980;20:632

206 Gregory GY 206001 Gya >99 X

206002 Hy >95 X

207 11 I 207001 I >99 X X * X 207002 i X

-

208 Er ER 208001 Era >99 208002 Erb <1

X Transfusion (Phila) 1982;22: 189 X Transfusion (Phila) 1988;28:268

209 209001 P >99 X X

209002 Pk X X

209003 LKE 98 X

* Vox Sang 1986;51:53; 1988;55:237; Hum Hered 1988;38:375

Descriptions and references to publications before 1975 may be found in Race and Sanger [6] for 201.2,3,5 & 6; 204.1; 205.1,3 & 4; 206.1 & 2:

Incidence (YO) refers to random cosmopolitan Caucasian populations; figures for other ethnic groups may be found in the references. By standard serological test, may appear to be low incidence.

207.1 & 2; 209.1, 2 & 3.

*

ISBT/ICSH Working Party 159

Table 6. The 700 Series: low incidence antigens not assigned to systems or collections

No. Name Symbol Reference

7oooO1 700002 700003 700004 700005 700006

700008

700010

700012 700013

700014 700015

700017 700018

7000 19 700020 700021 700022 700023

. . . . . . .

. . . . . . .

. . . . . . .

. . . . . . .

. . . . . . .

. . . . . . . 700026

700027 700028 700029 700030

70003 1 700032 700033 700034 . . . . . . . . . . . . . . 700037

. . . . . . . 700039 700040 700041

700043 700044 700045 700046 700047

. . . . . . .

Wright Batty Christiansen Swam Biles Box

Traversu

Bishop

Griffiths Wulfsberg

Nunhart Radin

Torkildsen Peters

Reid Ahonen Jensen Moen Hey

Froese

Redelberger Livesay Van Vugt Waldner

Duch POLL10

Hughes

NEW- FOUNDLAND

Miine Rasmussen

Oldeide

Katagiri Bowyer Jones

Wr"

Chra swa Bi Bxa

Tr"

BY"

BP"

Gf w u

Jn" Rd

To" Pt"

Re" An" Je" Mo" Hey

Fr"

Rb" Lia vga Wd"

Dh" POLL 0s" Hga

NFLD

RASM SWI

01" JFV

BOW Kg

Transfusion (Phila) 1988;28:113

Vox Sang 1988;54:184

Vox Sang 1980;39:225

Vox Sang 1976;31:337, 1980;38:213

Ann Hum Genet 1980;44:179

Vox Sang 1978;35:181; 1989;56: 112 Vox Sang 1985;49:400

Vox Sang 1982;43:31

Vox Sang 1978;35:251, Transfusion (Phila) 1980;20:217 Vox Sang 1978;35:397 Vox Sang 1980;38:305 Vox Sang 1981;41:48 Am J Hum Genet 1981;33:418; Am J Med Genet 1985;22:477 Hum Hered 1982;32:73 Clin Lab Haemat 1982;4:201 Vox Sang 1983;45:60 Vox Sang 1983;45:316

Hum Genet 1984;67:270; Hum Hered 1988;38: 122

Vox Sang 1984;47:290 Vox Sang 1986;51:133 Vox Sang 1987;52:115

Vox Sang 1986;50:235 Vox Sang 1988;55:44 Vox Sang 1989;56:98 Vox Sang 1988;55:241

JONES Vox Sang 1989;57:77

The 700 Series This series of computer numbers for low incidence anti-

gens ( 4 % in a random cosmopolitan Caucasian population) was created as a holding file. Each of the listed antigens (table6) is reportedly distinct from all other numbered low incidence antigens. Serological relationships between 700.4,26 & 41 and between 700.37 & 46 have been mentioned in the tabulated publications; as well as having unique epitopes Swa, Fra and SWI appear to share an epitope, as do NFLD and BOW. Unpublished data add 700.13 (Wu) to the NFLDBOW set [36] and indicate a serological relationship between 700.10 & 27 (Bpa and Rba) [37]. There is also some evidence of a genetic relationship between Swa and SWI.

The difficulty in obtaining enough information relative to blood group system exclusion, or inclusion, is obvious from the data displayed in table 7 where a blank indicates that families were either not informative or not tested. Antigen exclusion from a system is based on negative lods (-) at 0=0.00, i.e. at least one recombinant has been observed. Where no recombinant has been observed (+), the lods are small enough to be due to chance but, on the other hand, may portend a rewarding line of pursuit: Toa:ABO 0.90; Lia:LU 1.20 or 2.71, depending on the LU status of the untested grandparent; Lia:.7K 1.20; Osa: MNS 0.90; RASM:ABO 0.60; J0NES:RH 1.81; J0NES:JK 0.90. Because of the paucity of information about antigens en- countered in the families of only a few propositi, colleagues are encouraged to take advantage of current genetic and biochemical tools when investigating old or new members of the 700 Series (see resources below).

Ethnic nests have been identified for three of the five antigens that are near candidates for new systems: Radin, Froese and Waldner, and Wright and Swann. Rd is the only one that meets the stipulation of a chromosomal assignment (lp34-p32 [38]) but, since SC lies in the same region, exclusion or inclusion of Rd relative to the Scianna system will probably only be achieved at the molecular level.

Descriptions and references before 1975 may be found in Race and Sanger [6] for 700.1-23.

. . . . . . . Indicates an obsolete number; for the record they were initially used as follows: 700.7 for Lsa, now 201.6; 9 for Wb, now 201.5; 11 for Or, now MNS31; 16 for Heibel, controlled reagent no longer extant; 24 for RI", now equated with L S ~ [Green, Sistonen, Kornstad, Tippett, personal commun.]; 25 for Ina, now 203.1: 35 for Tch, now 202.3; 36 for Tc', now 202.4; 38 for Hov, now equated with Wu [Moulds, M. et al., personal commun.] and 42 for WES, now 202.8.

160 ISBTlICSH Working Party

Table 7. The 700 Series: genetic information relative to blood group systems*

No. Symbol Blood group system No.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19

The criteria for inclusion in the 700 Series are: (1) Distinction from all other numbered low-incidence anti-

(2) Demonstration of inheritance through at least two gen-

The 901 Series This Series is created as a holding file for antigens of

relatively high incidence (>90% in a random cosmopolitan Caucasian population) that have been neither assigned to any, nor excluded from all, of the established systems, and

gens.

erations.

ISBTDCSH Working Party 161

Table 8. The 901 Series: high-incidence antigens not assigned to systems or collections

References No. Name Symbol Incidence Excluded from systems Locus on % chromosome

901001 Vel >99 1 to 6 , 8 , 9 901002 Langereis Lan >99 1 to 4,6,8, 9 901003 August Ata >99 2 ,3 ,4 ,9 901004 Joseph Jo" >99 2,43798 Transfusion (Phila) 1976;16:531

Vox Sang 1978;35:265 901005 Jra >99 1 to 6,8, 9, 10 Ok" >99 1 to 4,7,8,9, 12,13, 17 19 Vox Sang 1979;36:182; 901006

Immunogenetics 1988;27:322 901007 JMH >99 Transfusion (Phila) 1978;18:387;

Transfusion (Phila) 1983;23:344 901008 Emm >99 Transfusion (Phila) 1987;27:319 901009 Anton AnWj >99 Vox Sang 1982;43:220;

Transfusion (Phila) 1983;23:128 901010 Fritz Wrb >99 Transfusion (Phila) 1976;16:396;

1988;28: 113 901011 MER2 92 1 to 9, 12,13,15, to 19 11 Cytogenet Cell Genet

1985;40:720; Vox Sang 1988;55:161

901012 Sid Sd" 91 1 to 4, 6,8,9, 12, 14, 19 901013 Duclos >99 Vox Sang 1978;34:302

Descriptions and references to publications before 1975 may be found in Race and Sanger [6] for 901.1,2,3,4,5,9 & 12.

do not fit into a Collection. The accumulated information is displayed in table 8.

The criteria for inclusion in the 901 Series are: (1) Distinction from all other numbered high incidence spe-

cificities. (2)Demonstration that the specificity is lacking in the red

cells of at least two sibs, i.e. that the negative phenotype is genetically determined.

Procurement of ISBT Numerical Designations

Choice of Symbol Symbols for designations of new specificities must not

duplicate, alphabetically or phonetically, any shown in the tables or any other that has been widely used but is now considered obsolete. To assist in the choice, an alphabet-- ical list of those to be avoided is appended (Appendix 1); the list includes some blood group phenotype and platelet antigen names, but symbols that are familiar to all have been omitted. Further, since prospective designations are restricted to a 3-6 on-line capital letter symbol, the list is

confined to those, some converted, that meet the numerical limitation.

Symbols for specificities that may herald new blood group systems, and thus new genes, have the further con- straint that they must differ from the symbols given to genes described in other disciplines. HGMNC gene symbol listings are updated daily; with FAX service, the originality of a proposed symbol can be assessed rapidly (consult Chair- man, M.L.).

Procedures for Acquisition of an ISBT Number The initial stipulation for the acquisition of an ISBT

number is that materials for 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 appended; they should be photocopied, completed, and forwarded to the appropriate Working Party member as indicated below.

For a 700 number: (1)Complete columns A and B of Appendix2. The list

includes antigens that would qualify as low incidence

162 ISBTDCSH Working Party

only in selected populations, e.g. KELl in Orientals. An incidence of 4 % in a random Caucasian population automatically distinguishes an antigen from LU1, KEL1, YT2 and C02.

(2)Completion of column C of Appendix 3 is optional. (3)Complete parts A and B of Appendix 4. Exclusion of an

antigen from a system automatically distinguishes it from low-incidence antigens in that system.

(4)Submit forms to Mr. J. J. Moulds who is authorized to assign a 700 number for a new, authenticated specificity.

For a 901 number: (1) Complete columns A and B of Appendix 3. (2)Completion of Column C of Appendix 2 is optional. (3)Complete parts A and B of Appendix 4. Exclusion of an

antigen from a system automatically distinguishes it from high incidence antigens in that system.

(4)Submit forms to Dr. G. L. Daniels who is authorized to assign a 901 number for a new, authenticated specificity.

For a specificity number in an established system: (1) For a low-incidence antigen, complete columns A and B

of Appendix 2, column C of appendix 3 for the pertinent blood group system and for the 700 and 901 Series.

(2)For a high-incidence antigen, complete column C of Appendix 2, and columns A and B of appendix 3 for the pertinent blood group system and for the 700 and 901 Series.

(3)For all antigens, complete parts A, B, and C of Appen- dix 4.

(4) Submit to Prof. Dr. W. Dahr for specificities in the MNS system, to Dr. P. D. Issitt for the Rh system, and to Dr. J. Jgrgensen for other systems.

For a specificity number in a current Collection: (1) For a low-incidence antigen, complete columns A and B

of Appendix2, and columns C of Appendix3 for the pertinent collection and for the 700 and 901 series.

(2)For a high incidence antigen, complete column C of Appendix 2, and columns A and B of Appendix 3 for the pertinent collection and for the 700 and 901 Series.

(3)For all antigens, complete parts A, B and D of Appen- dix 4.

(4)Submit forms to Dr. D. J. Anstee, Dr. G. L. Daniels or Mr. J . J . Moulds.

For a new blood group System or Collection: Proposals, with supporting data, should be submitted to

Prof. M. Lewis; decisions will be based on consensus of the full membership of the Working Party.

Resources

It was a relatively simple matter to establish individuality of the first few blood group systems and rare phenotypes. However, with the formation of systems comprised of products of genes that have polarized allele frequencies, exclusion of antigens from them and elucidation of new blood group systems have necessitated collaborative efforts. Blood group scientists have a long history of commu- nion, an element essential to the advancement of knowledge in our discipline. The SCARF (Serum, Cell and Rare Fluids) organization, co-ordinated by Mr. J. J. Moulds, has been particularly effective in perpetuating the free and regular exchange of materials, thereby facilitating the de- tection of new specificities, especially antigens of low incidence. Even so, it is unusual for any one laboratory to have the resources for complete investigation. We, there- fore, include this section to summarize consolidated resources that are available to all.

Serological There is long-standing co-operation between a network

of reference laboratories which store serum andlor red cells for identification of rare specificities. When materials are scarce, they are reserved for in-house testing; the use of this resource requires submission of a sample of the antibody- containing serum along with red cells carrying the low incidence antigen, or lacking the high incidence antigen, as pertinent. Most of the major reference laboratories are represented in the Working Party membership.

Genetic To realize the maximum amount of information from

families carrying a low incidence antigen, it is advantageous to use substitute markers for the blood groups that are not informative. A list of these markers is given in table 9; in each case the linkage between the blood group and substitute locus is so close that recombination seldom occurs. A 10-ml heparinized blood sample yields enough material for the examination of red cell, DNA and plasma polymorphisms; DNA is extracted by a simple procedure, is stable and easily transportable. Colleagues are urged to consult their local genetics laboratories to learn if testing for the desired marker is available or to utilize the RFLP testing offered by the Winnipeg Rh Laboratory. In either case, pre-arrangement is essential.

Several of the laboratories of Working Party members hold stored family samples informative for a number of blood group systems, rare types, and other genetic markers. These provide a ready source for genetic information

Table 9. Substitute markers for exclusion from Systems or Collec- tions

System Substitute

MNS Rh Lutheran Kell

Duffy

Kidd Scianna LW CWRG

Collection 201 (Gerbich) 202 (Cromer) 203 (Indian) 204 (Auberger)

~

GYPA [Cytogenet Cell Genet 1988;47:149] FLJCAl [Ann Hum Genet 1977;40:403] APOC2 [Ann Hum Genet 1988;52:137] L565RI-b [Cytogenet Cell Genet 1987;46:649] SPTAl [Hum Genet 1988;78:76; Cytogenet Cell Genet 1989;51:1042] D18S6 [Hum Genet 1987;77:205] MYCL [Genomics 1988;2:154]* LDLR [Ann Hum Genet 1988;52:137] HLA, C2, C4, BF [HGM3, Baltimore. Birth Defects Orig Art Ser 1975;12(7):307]

GYPC [Nucleic Acids Res 1987;15:1880] DAF [J Exp Med 1987;166:246] CD44' APOC2 [Vox Sang, in press]

163 ISBTKSH Working Party

gene or by contiguous, largely homologous, genes; there

All of the markers can be defined by or are restriction fragment length polymorphisms. * Assumed on the basis of chromosomal localization, and 6 for

' CD44 has recently been cloned [Cell 1989;56:1057-1062, 1063- 10721; presumably CD44 RFLPs will be described shortly.

RH:SC - 6 for R H : MYCL.

which might otherwise take decades for compilation. In particular, Drs. Daniels, Lewis, Lubenko, Okubo and Tip- pett offer in-house testing if supplied with an adequate amount of reagent.

Biochemical As already indicated, biochemical studies have been

instrumental in the formation of Collections 201, 202 and 203. They have also revealed the nature of integral relationships of MNS system specificities [e.g. 39, 40, 411, and confirmed the serological assignment of some specificities to the Kell system [42]. Approximate molecular weights for some of the red cell antigen carrying proteins are set out in table 10.

A variety of biochemical techniques can be used, immu- noblotting and immunoprecipitation having been the most successful. Drs. Anstee, Dahr and Daniels offer advice and/or assistance on request.

Conclusion

We have classified serologically determined red cell antigens/specificities into three categories according to present knowledge: Systems, Collections and Series. Each Sys- tem is composed of those that are controlled by a single

Table 10. Approximate molecular weights of some red cell antigen carrying proteins

Protein MW, kD Reference System

MNS GYPA 37 Biochim Biophys Acta 1975;382:172 GYPB 25 Biochim Biophys Acta 1975;382:172

Rh D protein 30 FEBS Lett 1982;140:93 c protein 30 Nature 1982;295:529 E protein 30 Nature 1982;295:529

Lutheran Lub 85 & 78 Transfusion (Phila) 1987:27:61 Kell 93 Transfusion (Phila) 1984;24: 176

LW LW"b 42 JP Cartron et al (eds): Red Cell Membrane Glycoconjugates and

CWRG c 4 200 Biochem J 1977;165:439 Kx 37 Br J Haematol 1988;68:131

Collection Gerbich GYPC/D 35 & 27 Biochem J 1987;244:123 Cromer DAF 70 Immunology 1987;62:307 Indian CD44 80 Immunology 1988;64:37

50 Nature 1982;295:529 Duffy FYa

Related Genetic Markers. Paris, Arnette 1983, p97

164 ISBTfICSH Working Party

are 19 distinct Systems. The 9 Collections are comprised of specificities that have a serological, biochemical or genetic connection. Finally, the 700 and 901 Series consist of 38 low and 13 high incidence specificities respectively; the constituents have not been assigned to Systems or Collections because of either exclusion from, or lack of information about, some or all of them.

We have summarized present genetic information that supports the individuality of the 19 Systems, and detailed the basis for inclusion of specificities in the 9 Collections. As well, we have reviewed the demonstrated use and po- tential value of current genetic and biochemical tools in the elucidation of Systems and of integral relationships between specificities.

On the basis of the above categorizations, we have struc- tured a six-digit numerical specificity designation for computer use; this designation is tabulated along with conventional counterparts and an alternative alphabeticallnumerical system, based on the six-digit system, for textual and verbal use. The choice of terminology is the prerogative of any author. However, the success of the Working Party in maintaining at least numerical order, is dependent on the cooperation of members of the blood-grouping community, and, to this end, we urge acquisition of ISBT numbers for inclusion in initial publications.

Guidelines for the inclusion of specificities, old or new, in any of the categories, and for the procurement of an ISBT number are set out in detail. We hope that strict adherence to these guidelines will prevent the future inad- vertent use of the same name for different specificities and of different names for the same specificity. The official notification of allocation of an ISBT number will validate the singularity and/or classification of the designated specificity.

Addresses and FAX numbers for members of the Work- ing Party are listed in Appendix5; all members are pre- pared to handle requests for advice or assistance in any aspect of an investigation or to direct them to the most appropriate authority. Membership in the Working Party is open to colleagues who wish to participate actively in delib- erations.

Acknowledgements

We are indebted to past members for their contributions: Dr. P. Booth, Dr. E. Freiesleben, Dr. 0. K. Gavrilov, Dr. C. F. Hogman, Dr. J. Leikola, Dr. E. Lisowska, Dr. F, Lothe, Mrs. B. Sabo, Dr. T. B. Shows, Dr. S. M. Smythe and Dr. J. Yasuda. The Chairman is grateful to her Research Associate, Sylvia Philipps, for preparing, revising and processing the computerized listings that have served as our working papers.

~~

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

19

20

21

References

Rosenfield RE, Allen FH, Swisher SN, et al: A review of Rh serology and presentation of a new terminology. Transfusion (Phi- la) 1962;2:287. Allen FH Jr, Anstee DJ, Bird GWG, et al: ISBT Working Party on Terminology for Red Cell Surface Antigens. Preliminary Report. Vox Sang 1982;42:164. Allen FH Jr: Report of the ISBT Working Party on Terminology for Red Cell Surface Antigens. ISBT Newslett No 18, April 1983. Lewis M, Allen FH Jr, Anstee DJ, et al: ISBT Working Party on Terminology for Red Cell Surface Antigens. Munich Report. Vox Sang 1985;49;171. Lewis M: The Working Party on Terminology for Red Cell Surface Antigens. ISBT Newslett No 34, April 1987. Race RR, Sanger R: Blood Groups in Man, ed 6. Oxford, Black- well, 1975. Issitt PD: Applied Blood Group Serology, ed 3. Miami, Mont- gomery Scientific Publications, 1985. Shows TB, McAlpine PJ, Boucheix C, et al: Guidelines for human gene nomenclature. Human Gene Mapping 9, Paris 1987. Cytoge- net Cell Genet 1987;46:11-28. Sistonen P, Nevanlinna H, Virtaranta-Knowles K, et al: Ne”, a new blood group antigen in Finland. Vox Sang 1981;40:352. Sistonen P, Tippett P: A ‘new’ allele giving futher insight into the LW blood group system. Vox Sang 1982;42:252. Sistonen P: Linkage of the LW blood group locus with the complement C3 and Lutheran blood group loci. Ann Hum Genet 1984; 48;239. Giles CM: ‘Partial inhibition’ of anti-Rg and anti-Ch reagents. 11. Demonstration of separable antibodies for different specificities. Vox Sang 1985;48:167. Giles CM: Three Chido determinants detected on BSRg+ allotype of human C4: their expression in Ch-typed donors and families. Hum Immunol1987;18:111. Giles CM, Jones J W A new antigenic determinant for C4 of relatively low frequency. Immunogenetics 1987;26:392. Salmon Ch, Cartron J-P, Rouger Ph: The Human Blood Groups. Paris, Masson, 1984. Francke U, Ochs HD, de Martinville B, et al: Minor Xp21 chromosome deletion in a male association with expression of Duchenne muscular dystrophy, chronic granulomatous disease, retinitis pigmentosa and McLeod syndrome. Am J Hum Genet 1985; 37:250. Bertelson CJ, Pogo AO, Chaudhuri A, et al: Localization of the McLeod locus (Xk) within Xp21 by deletion analysis. Am J Hum Genet 1988;42:703. Redman CM, Marsh WL, Scarborough A, et al: Biochemical studies on McLeod phenotype red cells and isolation of Kx antigen. Br J Haematol 1988;68:131. Anstee DJ, Ridgwell K, Tanner MJA, et al: Individuals lacking the Gerbich blood-group antigen have alterations in the human erythrocyte membrane sialoglycoproteins p and y. Biochem J 1984; 221 : 97. Colin Y, Le Van Kim C, Tsapis A, et al: Human erythrocyte glycophorin C. Gene structure and rearrangement in genetic variants. J Biol Chem 1989;264:3773. Mattei MG, Colin Y, Le Van Kim C, et al: Localization of the gene for human erythrocyte glycophorin C to chromosome 2q14-q21. Hum Genet 1986;74:420.


22 Sistonen P: Some notions on clinical significance of anti-Lsa and independence of Ls from Colton, Kell and Lewis blood group loci (abstract). 19th ISBT Proc, Sydney 1986, p 652.

23 Spring FA, Judson PA, Daniels GL, et al: A human cell-surface glycoprotein that carries Cromer-related blood group antigens on erythrocytes and is also carried on leucocytes and platelets. Immu- nology 1987;62:307.

24 Telen MJ, Hall SE, Green AM, et al: Identification of human erythrocyte blood group antigens on decay-accelerating factor (DAF) and an erythrocyte phenotype negative for DAE J Exp Med 1988;167:1993.

25 Rey-Campos J, Rubinstein P, Rodriquez de Cordoba S: Decay- accelerating factor. Genetic polymorphism and linkage to RCA (regulator of complement activation) gene cluster in humans. J Exp Med 1987;166:246.

26 Daniels GL, Green CA, Darr FW, et al: A ‘new’ Cromer-related high-frequency antigen probably antithetical to WES. Vox Sang 1987;53:235.

27 Lewis M, Kaita H, Philipps S, et al: Exclusion of unassigned blood group system loci from the RCA gene cluster on lq32. Vox Sang 1989;57:210.

28 Spring FA, Dalchau R, Daniels GL, et al: The Ina and Inb blood group antigens are located on a glycoprotein of 80,000 MW (the CDw44 glycoprotein) whose expression is influenced by the In(Lu) gene. Immunology 1988;64:37.

29 Tippett P, Daniels GL, Green CA, et al: Genetic independence of Aun from the loci for Kell and Colton blood group systems. Trans- fusion (Phila) 1988;28:20S.

30 Kaita H, Lewis M, Moulds JJ: Unpublished data. 31 Zelinski T, Kaita H, Johnson K, et al: Genetic evidence that the

gene controlling Aub is located on chromosome 19. Vox Sang 1990;58: 126-128.

32 Daniels GL: Evidence that the Auberger blood group antigens are located on the Lutheran glycoproteins. Vox Sang 1990: 5856-60.

33 Molthan L: Unpublished data submitted to the Working Party. 1985.

34 Moulds JJ, Polesky HF, Reid M, et al: Observations on the Gy” and Hy antigens and the antibodies that define them. Transfusion (Phi- la) 1975;15:270.

35 Fellous M, Hors MC, Rebourcet R, et al: The expression and relation of HLA, &microglobulin and receptor for marmoset red cells on man/mouse and man/Chinese hamster hybrid cells. Eur J Immunol 1977;7:22.

36 Moulds M, Kaita H, Kornstad L, et al: Unpublished data. 37 Poole J, Giles CM: Unpublished data. 38 Lewis M, Kaita H, Philipps S, et al: The position of the Radin blood

group locus in relation to other chromosome 1 loci. Ann Hum Genet 1980;44:179.

39 Anstee DJ, Mawby WJ, Parsons SF, et al: A novel hybrid sialoglycoprotein in Sta positive human erythrocytes. J Immunogenet 1982;9:51.

40 Dahr W, Kordowicz M, Judd WJ, et al: Structural analysis of the Ss sialoglycoprotein specific for the Henshaw blood group from human erythrocyte membranes. Eur J Biochem 1984; 14151.

41 Dahr W, Beyreuther K, Moulds J: Hybrid glycophorins from human erythrocyte membranes. I. Isolation and complete structural analysis of the hybrid sialoglycoprotein from Dantu-positive cells of the N.E. variety. Eur J Biochem 1987;166:31.

42 Marsh WL, Redman CM, Kessler LA, et al: K23. A low-incidence antigen in the Kell blood group system identified by biochemical characterization. Transfusion (Phila) 1987;27:36.

Prof. Marion Lewis Rh Laboratory 735 Notre Dame Ave. Winnipeg, Canada R3E OL8

Addenda

Terminology: For publications in which italic print is not used, an asterisk must be inserted between the alphabetical symbol and the number in allele and genotype designations, e.g. JK*l, JK*2 and JK*V2.

Blood Group Systems. 002 (MNS). The Human Gene Mapping Nomenclature Committee has adopted the terms GYPA (glycophorin A) and GYPB (glycophorin B) for the M N and Ss loci respectively [McAlpine PJ, Shows TB, BoucheixC et al: HGMlO (New Haven, 1989). Cytogenet Cell Genet 1989;51:13-66]. Our Working Party rec- ommends that ‘blood groupers’ continue to use the conventional symbol MNS.

015 (Colton). The CO locus has been linked to the argininosucci- nate synthetase pseudogene 11 locus (ASSPll) on chromosome 7p: i = 5.79 at 6 = 0.07 [Zelinski T, Kaita H, Gilson T, et al: Genomics, in press].

018 (H) The HGMNC has adopted the term FUTl (fucosyl transferase 1) in place of H [see reference in 002 above]. As a matter of interest, they have adopted the term FUT2 (fucosyl transferase 2) as a replace- ment for SE (the secretor locus).

Blood Group Collections: 204 (Auberger) . The genetic and biochemical relationships of the AU antigens have been the topics of Abstracts [Zelinski T, Kaita H, Moulds M: Transfusion 1989;29:S42, 16s and Daniels GL: Transfusion 1989;29:S114, 34S, respectively].

The 700 Series: Three new low-incidence antigens are under review for 700 numbers: FPTT [Bizot M, Lomas C, Rubio F, et al: Transfusion 1988;28:342], HJK [McCreary, p.c.1, HOFh4 [Hoffman JJML, Over- beeke MAM, Kaita H et al, p.c.1.

The 901 Series: 009 (Anton). The AnWj antigen now meets the inheritance requirement [Poole J, Levene C, van Alphen L et al, Transfusion 1989;29:S115, 34Sl.

Appendixl: The terms Bra and Brb have been used for a new platelet alloantigen system [Santoso S, Kiefel V, Mueller-Eckhart C. Haematol1989;72:191; consequently, BRA and BRB should be added to the list of ‘used’ symbols along with FPTT, HJK and HOFM mentioned above in the 700 series.

Appendix 2: Assignment of a number will also require distinction from the new antigens mentioned above.

Appendix 4: The printed reproduction of Appendix 4 may be too small for the inclusion of all supporting information; in that event, applicants should append extra pages.

166 ISBTIICSH Working Party

Appendix 1

Alphabetical List of ‘Used’ Symbols or Names

AEL AEND AHONEN AINT ANA ANEK ANTON ANWJ ATA AUGUST BAK BARNES BATN BEA BEAL BEC BECKER BEL BGA BGB BGC BILES BISHOP BOC BOW BOWYER BOX BPA BUA

BULLEE BXA CAD CAN CENT CHRA CLA CLAAS CLS COST COTE CROMER CSA CSB DAF DANTU DAV DAY DEAL DELCOL DEN DHA DON DONNA DRA DREYER DUCH DUCLOS DUZO

EL0 EMM ENA ENAFR ENAFS ENATS ERA ERB ESA ESP EVANS FAR FRA FRITZ FROESE GARY GILL GOA GOOD GYA GYPA GYPB GYPC HAR HEIBEL HEY HGA HIL

HILL HOF HOLLEY HOP HOV HTA HUGHES HUNT HUNTER HUT IFC IKAR INA INAB INB INDIAN INLU JAL JAN JARVIS JCA JEA JENSEN JFV JMH JNA JOA JOB JONES

JOSEPH JRA KAM KIR KNA KNB KNOPS LAN LANE LEACH LEK LEVAY LIA LKE LOX LSA LUD LUKE MARTIN MCCA MCCOY MCLEOD MER MIDDEL MIL MILNE MIT MOA MOEN

MTA MUCH MULL MUR NAK NEA NFLD NOB NOR NOU NYA NYBERG OCA OKA OLA ORRISS OSA PELTZ PENNEY PETERS PLA POLL10 JTA RADIN RADDON RAF RASM RBA REA

REID REITER RIA RIDLEY RIV RLA ROB SALIS SAN SDA SEC SFA SGRO SIB SID SKA SLA STA STOBO STONES SUB SUL SUTTER SWA SWANN SWI SYN TAR TAYLOR

TCA TCB TJA TOA TOFTS TRA TROLL TSUNOI ULA UMC UPR UPS VEL VEN VGA WDA WEBB WEEKS WES WIEL WKA WRA WRB WRIGHT YAHUDA YKA YORK YUK YUS

Appendix 2

Application for ISBT Number For low-incidence antigen: Column A: indicate + or - for result of testing ‘new’ antibody with cells carrying numbered antigen. Column B: indicate + or - for result of

For high-incidence antigen: Column C: indicate + or - for result of testing cells of ‘new’ antibody producer with antibody specific for numbered antigen.

testing ‘new’ antigen with antibody specific for numbered antigen.

ISBTKSH Working Party 167

Appendix 2 cont

Appendix 3

Application for ISBT Number For high-incidence antigen: Column A: indicate + or - for result of testing ‘new’ antibody with cells negative for numbered specificity. Column 8: 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 result of testing ‘new’ antibody with cells negative for numbered specificity.

Proposed symbol Incidence Proposed name

A B C A B C A B C A B C

CWRGl - - - 206.1 - - - 206.2 ~ __ ~ CWRG2 - - -

CWRG3 - - - 207.1 __ __ - CWRG4 - - - 207.2 - - - CWRG5 - - __ 208.1 __ - -

209.1 __ __ __ CWRG6 - - __ KEL13 - __ - CWRGll- __ __ 209.3 __ __ -

MNS5 - - - KEL2 - - - MNS28 - - KEL4 - - - MNS2Y - ~ - KEL5 - _. - RH17 - - - KEL7 - - - RH18 __ - - KELll - - - RH29 - - - KEL12 - __ -

RH34 - - -


Appendix 3 cont.

RH44

RH46

RH47

LU2

LU3

LU4

LU5

LU6

LU7

LU8

L u l l

LU12

LU13

LU16

LU17

KEL14

KEL16

KEL18

KEL19

KEL20

KEL22

FY3

N 5

JK3

D12

YT1

sc1 s c 3

co1 C 0 3

LW5

LW6

CWRG12 - H1 - XKl - 201.2 - 201.3 - 201.4 - 202.1 - 202.2 - 202.5 - 202.6 - 202.7 - 202.9 - 202.10 - 203.2 - 205.1 - 205.3 - 205.4 - 205.6 - 205.7 -

901.1

901.2

901.3

901.4

901.5

901.6

901.7

901.8

901.9

901.10

901.11

901.12

901.13

Investigator: Date:

Appendix 4 D. Inclusion in a collection: collection name

Application for ISBT Number.

Genetic:

Serological:

Biochemical: Proposed Name Proposed Symbol

Ai . Aii . B.

C.

Inheritance: ratio + : - offspring

Inheritance: ratio + : - siblings Exclusion from blood group systems: List systems and z counts' for each List substitute markers and z counts for each

Inclusion in a system: system name

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

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.

Biochemical: ' Consult Race and Sanger [6, pp. 552-5591 for determination.


Appendix 5

Addresses and FAX Numbers of Working Party Members

Dr. D. J. Anstee: Blood Group Reference Laboratory, Regional Transfusion Centre, Southmead Road, Bristol BSlO 5ND, UK. FAX 0272 591 660

Dr. G. W. G. Bird: Regional Blood Transfusion Centre, Vincent Drive, Edgbaston, Birmingham B13 9XH, UK

Dr. E. Brodheim: Columbia University, Dept. of Industrial Engineer- ing and Operations Research, Room 308, Mudd Building, New York, NY 10027, USA. FAX (212) 3169068

Dr. J.-P. Cartron: INTS, 6, rue Alexandre-Cabanel, 75739 Pans Cedex 15, France

Dr. M. Contreras: North London Blood Transfusion Centre, Colindale Ave., London, NW9 5BG, England. FAX 01-2003994

Mrs. M. C. Crookston: 246 Russell Hill Road, Toronto, Ontario, M4V 2T2, Canada

Prof. Dr. W. Dahr: Stein-Strasse 4, D-5060 Bergisch Gladbach 1, FRG Dr. G. L. Daniels: MRC Blood Group Unit, Wolfson House, 4 Ste-

phenson Way, London NW12HE, UK, FAX 01-3882374 Prof. Dr. C. P. Engelfriet: PO Box 9190 NL, 1006AD, Amsterdam, The

Netherlands. FAX 20-5123332 Dr. C. M. Giles: Rheumatology Unit, Hammersmith Hospital, Du

Cane Road, London W E OHS, UK. FAX 01-7403169 Dr. P. D. Issitt: Room 131 Carl Building, Transfusion Service, Duke

University Medical Center, PO Box 2928, Durham NC 27710, USA. FAX (919) 684 3589

Dr. J. Jergensen: University Hospital, Skejby, Denmark DK-8200.

Dr. L. Kornstad: Statens Institute for Folkeshelse, Dept. of Immunol- ogy, National Blood Group Reference Laboratory, Geitmyrsveien 75,0462 Oslo 4, Norway. FAX 472-353605

Prof. M. Lewis: Rh Laboratory, 735 Notre Dame Ave., Winnipeg, Man. R3E OL8, Canada. FAX (204) 787-4807

Dr. A. Lubenko: North London Blood Transfusion Centre, Colindale Ave., London, NW9 5BG, UK. FAX 01-2003994

FAX 045-6 78 40 16

Dr. W. L. Marsh: New York Blood Center, 310 E 67 St., New York, NY 10021, USA

Mrs. J. McCreary: Ortho Diagnostics Inc., Raritan, NJ08869, USA. FAX (201) 218 8582

Dr. B. P. L. Moore: Canadian Red Cross Blood Services, Toronto Cen- tre, 222 St-Patrick St., Toronto, Ont. M5T 1V4, Canada. FAX (416) 974 9851

Mrs. P. Morel: Delta Blood Bank, P.O. Box 230, Stockton, CA 95201- 9973, USA

Mr. J. J. Moulds: Gamma Biologicals Inc., 3700 Mangum Rd., Hous- ton, TX 77092, USA. FAX (713) 956 3333

Prof. Dr. H. R. Nevanlinna: Finnish Red Cross Blood Transfusion Ser- vice, Kivihaantie 7, SF-00310, Helsinki 31, Finland. FAX 5801 329

Dr. R. Nordhagen: Statens Institute for Folkehelse, Geitmyrsveien 75, 0462 Oslo 4, Norway. FAX 472 353605

Dr. Y. Okubo: Osaka Red Cross Blood Center, 4-34 Morinomiya, 2-Chome, Joto-Ku, Osaka 536, Japan. FAX 06-968-4900

Dr. R. E. Rosenfield: Box 1079, Mount Sinai Medical Center, One Gustave Levy Place, New York, NY 10029, USA

Dr. Ph, Rouger: Centre National de Reference pour les groupes San- guines. CNTS St Antoine, 53, boulevard Diderot, 75571 Paris Ce- dex 13, France

Dr. P. Rubinstein: New York Blood Center, 310 E67 St., New York, NY 10021, USA

Prof. Dr. Ch. Salmon: INTS, 6 rue Alexandre-Cabanel, 75739 Paris Cedex 15, France

Prof. Dr. S. Seidl: Blutspendedienst Hessen, Sandhofstrasse 1, PB 730367, D-6000 Frankfurt AM 71, FRG. FAX (069) 6782110

Dr. P. Sistonen: Finnish Red Cross Blood Transfusion Service, Kivi- haantie 7, SF-00310, Helsinki 31, Finland. FAX 5801 329

Dr. P. Tippett: MRCBlood Group Unit, Wolfson House, 4 Stephenson Way, London NW12HE, UK. FAX 01-388 2374

Dr. R. H. Walker Wm.: Beaumont Hospital, 3601 West 13 Mile Rd., Royal Oak, MI 48072, USA

Dr. G. Woodfield: New Zealand Blood Transfusion Services, Park Avenue, Auckland 1, New Zealand. FAX 09-790985

Mr. S. Young: Australian Red Cross Society, Blood Transfusion Ser- vice, 301 Pine St., Adelaide 5000, Australia. FAX 08-223 7280

blood group terminology 1990 - isbt: international … cells/reports... · vox sang....

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