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Vox Sang. 1990;58:152-169 Section Editors: M . Garretta, Les Ulis C. E Hogman, Uppsala Blood Group Terminology N901 From the ISBT Working Party on Terminology for Red Cell Surface Antigens 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 Terminology for Red Cell Surface Antigens was initiated by Dr. B. P. L. Moore on the recommendation of the ISBT Working Party on Automation and Data Processing. The mandate 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 unanimous agreement that existing terminology would not be altered, but that designations for genes/loci, for the alphabeticahumerical 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. Allen (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. Allen, 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 documenting 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 instances, 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- ISBT/ICSH Working Party 153 Table 1. Designations for blood group systems and antigen specificities Name Symbol No. ABO ABO MNS MNS P P1 Rh Lutheran Kell Lewis Duffy Kidd Diego Yt xg Scianna Domhrock Colton Landsteiner-Wiener Chido/Rodgers Hh Kx RH LU KEL LE FY JK DI YT XG SC DO CO LW CWRG H XK No. within system 001 002 003 001 002 A M B N A,B A1 S s 003 004 P1 005 006 007 008 009 010 011 012 013 014 015 016 017 018 019 D Lu" K Lea Fya Jk" Dia Yt" Xga Sm Do" Coa 004 ...... C E Lub Luab k Kp" Leb Leab Fyb Fy3 Jkb Jkab Dib Ytb 005 006 007 008 009 010 011 He Mi" M Vw Mur Me 012 013 014 015 016 017 V' Me Mta St" Ria Cl' .., U e f Ce Cw Cx V EW G RhA RhB RhC RhD Hr,, Lu4* LuS* Lu6* Lu7* Lug* Mull Lull*Much Hughes Lu14* Lu16 Lui7* Kpb KU Js" Jsb U1" Cote BBc' K13* Sans 'k-like' Wka c ...... Fy4 Fy' ... ... ... Fy6 Bu" SC' Dob Cob Coab ............ LWa LWab LWb Chl Ch2 Ch3 Ch4 ChS Ch6 WH H Kx Rgl Rg2 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). indicates that a number is now obsolete, the specificity having been removed altogether because of inadequate documentation or to another 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. * 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 alphabeticalhumerical 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 1to 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 understood that system 7 refers to serologically defined products of the L E 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 154 ISBT/ICSH Working Party Table 2. Extension of blood group system specificities No. within system System symbol System No. 018 019 020 021 022 MNS 002 NY" Hut Hi1 MV Far 023 SD 024 Mit 02s 026 027 028 029 Dantu HOP Nob Ena En"KT 030 " 031 032 Or Reference System symbol System No. RH 004 Hr hrs CG CE DW K23* ET CIS vs 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. System symbol System No. KEL 006 K18* Sub* Km KP' K22* ... Reference 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 e-like cE hrH 'total Rh' Goa hrB Rh32 033 034 035 036 037 038 039 Har HrB* Rh35* Be" Evans 040 Tar 041 Rh41 042 Cces* 043 Crawford 044 Nou 045 Riv 046 Sec 047 Dav 048 JAL * Reference ... Rh39 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 Immunohaematol 1981;24:117. Transfusion (Phila) 1983;23:410. Transfusion (Phila) 1989;29:798. Blood Transfus Immunohaematol1982;25:18S. Poole J et al: personal commun. Descriptions of specificitiesnot 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 recommendationsof the author. ... ISBTIICSH Working Party 155 Table 3. Sample phenotype and genotype designations System Colton Traditional Alternative Phenotype Co(a+b-) co:1,-2 Genotype coalco" or or CO"lC0 co 110 Phenotype Co(a+b+) c0:1,2 Genotype Co"lCoh co 112 Phenotype Co(a-b+) c0:-1,2 Co~lCo~ co 212 Genotype or or COhlCO co 210 Phenotype Co(a-b-ab-) c0:-1, -2, -3 Genotype COlCO co 010 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 co I l l ~ Kell 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 documented 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 1,2,5and 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 156 ISBT/ICSH Working Party Table 4. Chromosomal locations of blood group system genes Chromosome 1 1 4 6 9 18 19 19 22 X 9 Arm Locus, region 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), followedby the region, and then by the band within the region, in both cases numbered from the centromere. ter = end. The first indications of a chromosomal assignment are referenced; for refinements consult the pertinent Committee Report in Human Gene 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 extent 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 difference 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 ‘polymorphic’ 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. Guidelinesfor 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 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 characterized 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 implied by the symbols; these have not been substantiated by population statistics indicating Hardy-Weinberg expectation or by Mendelian ratios of offspring phenotypes in the various mating types, but the incidence of Tcbin 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 cotrolled by the DAF gene as well as being carried on its protein, classical family studies with 202.8 (WES”) as the 157 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 Auberger 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 dihexoside), 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 antigenshpecificitieswith serological, biochemical or genetic connections Collection Specificity Connection Reference No. name symbol No. symbol inciserobiochem- genetic dence % logical ical 201 Gerbich GE 201002 201003 201004 201005 201006 Ge2 Ge3 Ge4 Wb Ls" >99 >99 >99 <1 <I Cra Tc" Tcb Tcc Dra Esa IFC WES" WESb UMC >99 299 <1 <1 >99 >99 >99 <1 >99 >99 202 Cromer CROMER 202001 202002 202003 202004 202005 202006 202007 202008 202009 202010 X X X X X 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 X X X X X X X X X X X X X X X X X X X Transfusion (Phila) 1975;15:522 Transfusion (Phila) 1983;23:124 Transfusion (Phila) 1982;22:413; 1985;25:373 Transfusion (Phila) 1982;22:413 Transfusion (Phila) 1984;24:13; 1987;27:64 Abst XVIII ISBT p 163, 1984 Transfusion (Phila) 1988;28:427 Vox Sang 1987;52:111 Vox Sang 1987;53:235 Transfusion (Phila) 1989;29:794 ~~ 203 Indian IN 203001 Ina 203002 Inb <1 >99 X X X X Vox Sang 1974;26;400 Vox Sang 1975;29:73 -__- 204 205 206 207 Auberger AU 204001 Au" 204002 Aub 90 50 X X Vox Sang 1982;43:259 Vox Sang 1989;56:54 ~ Cost Gregory 11 COST GY I 205001 205002 205003 205004 205005 205006 205007 Cs" Csb Yk" Kn" Knb McCa SI" 95 34 95 >99 5 >99 99 X 206001 Gya 206002 Hy >99 >95 X 207001 I 207002 i >99 208001 Era 208002 Erb >99 <1 209001 P 209002 Pk 209003 LKE >99 * X X __ Am J Med Tech 1983;49:49 Med Lab Sci 1987;44:94 Vox Sang 1975;29:145 X x Transfusion (Phila) 1980;20:630 Transfusion (Phila) 1978;18:566 Transfusion (Phila) 1980;20:632 X Transfusion (Phila) 1982;22:189 Transfusion (Phila) 1988;28:268 X X X X X X X - 208 209 Er ER X * X X X X 98 X Vox Sang 1986;51:53; 1988;55:237;Hum Hered 1988;38:375 Descriptions and references to publicationsbefore 1975 may be found in Race and Sanger [6] for 201.2,3,5 & 6; 204.1; 205.1,3 & 4; 206.1 & 2: 207.1 & 2; 209.1, 2 & 3. 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. 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 Wright Batty Christiansen Swam Biles Box Wr" BY" Chra swa Bi Bxa Traversu Tr" Bishop BP" ....... 700008 ....... 700010 ....... 700012 Griffiths 700013 Wulfsberg Gf wu 700014 Nunhart 700015 Radin Jn" Rd 700017 Torkildsen 700018 Peters To" Pt" ....... 700019 700020 700021 700022 700023 ....... ....... Reid Ahonen Jensen Moen Hey Re" An" Je" Mo" Hey 700026 Froese Fr" 700027 700028 700029 700030 Rb" Lia vga Wd" Redelberger Livesay Van Vugt Waldner 700031 Duch 700032 POLL10 700033 700034 Hughes ....... ....... Dh" POLL 0s" Hga NFLD 700037 NEWFOUNDLAND ....... 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 700039 Miine 700040 Rasmussen 700041 Vox Sang 1984;47:290 RASM Vox Sang 1986;51:133 Vox Sang 1987;52:115 SWI 700043 700044 700045 700046 700047 Oldeide 01" Katagiri Bowyer Jones JFV Kg BOW JONES ....... Vox Sang 1986;50:235 Vox Sang 1988;55:44 Vox Sang 1989;56:98 Vox Sang 1988;55:241 Vox Sang 1989;57:77 The 700 Series This series of computer numbers for low incidence antigens ( 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 (Bpaand 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:.7K1.20; Osa:MNS 0.90; RASM:ABO 0.60; J0NES:RH 1.81; J0NES:JK 0.90. Because of the paucity of information about antigens encountered 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 ~ Sistonen, Kornstad, extant; 24 for RI", now equated with L S [Green, 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 The criteria for inclusion in the 700 Series are: (1) Distinction from all other numbered low-incidence antigens. (2) Demonstration of inheritance through at least two generations. 7 8 9 10 11 12 13 14 15 16 17 18 19 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 ISBTDCSH Working Party 161 Table 8. The 901 Series: high-incidence antigens not assigned to systems or collections No. Name Symbol Incidence Excluded from systems % 901001 901002 901003 901004 901005 901006 Langereis August Joseph 901007 Vel Lan Ata Jo" Jra Ok" >99 >99 >99 >99 >99 >99 JMH >99 901008 901009 Anton Emm AnWj >99 >99 901010 Fritz Wrb >99 901011 901012 901013 MER2 Sid Duclos Sd" 92 91 >99 Locus on chromosome 1 to 6 , 8 , 9 1 to 4,6,8, 9 2,3,4,9 2,43798 1to 6,8, 9, 10 1 to 4,7,8,9, 12,13, 17 19 1to 9, 12,13,15, to 19 11 References Transfusion (Phila) 1976;16:531 Vox Sang 1978;35:265 Vox Sang 1979;36:182; Immunogenetics 1988;27:322 Transfusion (Phila) 1978;18:387; Transfusion (Phila) 1983;23:344 Transfusion (Phila) 1987;27:319 Vox Sang 1982;43:220; Transfusion (Phila) 1983;23:128 Transfusion (Phila) 1976;16:396; 1988;28:113 Cytogenet Cell Genet 1985;40:720; Vox Sang 1988;55:161 1 to 4 , 6 , 8 , 9 , 12, 14, 19 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 specificities. (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 constraint 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 Chairman, 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 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 Appendix 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 Appendix 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. ISBTDCSH 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 communion, 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 detection 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, therefore, 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 antibodycontaining 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 ISBTKSH Working Party 163 Table 9. Substitute markers for exclusion from Systems or Collec- tions System Substitute ~ MNS Rh Lutheran Kell Duffy Kidd Scianna LW 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] CWRG Collection 201 (Gerbich) 202 (Cromer) 203 (Indian) 204 (Auberger) GYPC [NucleicAcids Res 1987;15:1880] DAF [J Exp Med 1987;166:246] CD44' APOC2 [Vox Sang, in press] All of the markers can be defined by or are restriction fragment length polymorphisms. * Assumed on the basis of chromosomal localization, and 6 for RH:SC 6 for R H : MYCL. CD44 has recently been cloned [Cell 1989;56:1057-1062, 106310721; presumably CD44 RFLPs will be described shortly. - ' which might otherwise take decades for compilation. In particular, Drs. Daniels, Lewis, Lubenko, Okubo and Tippett 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, immunoblotting 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 System is composed of those that are controlled by a single gene or by contiguous, largely homologous, genes; there Table 10. Approximate molecular weights of some red cell antigen carrying proteins System Protein MW, kD Reference MNS GYPA GYPB D protein c protein E protein Lub 37 25 30 30 30 85 & 78 93 50 42 Rh Lutheran Kell Duffy LW CWRG Kx Collection Gerbich Cromer Indian c4 200 37 Biochim Biophys Acta 1975;382:172 Biochim Biophys Acta 1975;382:172 FEBS Lett 1982;140:93 Nature 1982;295:529 Nature 1982;295:529 Transfusion (Phila) 1987:27:61 Transfusion (Phila) 1984;24:176 Nature 1982;295:529 JP Cartron et al (eds): Red Cell Membrane Glycoconjugates and Related Genetic Markers. Paris, Arnette 1983, p97 Biochem J 1977;165:439 Br J Haematol 1988;68:131 GYPC/D DAF CD44 35 & 27 70 80 Biochem J 1987;244:123 Immunology 1987;62:307 Immunology 1988;64:37 FYa LW"b 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 potential 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 structured 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 inadvertent 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 Working Party are listed in Appendix5; all members are prepared 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 deliberations. 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. References 1 Rosenfield RE, Allen FH, Swisher SN, et al: A review of Rh serology and presentation of a new terminology. Transfusion (Phila) 1962;2:287. 2 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. 3 Allen FH Jr: Report of the ISBT Working Party on Terminology for Red Cell Surface Antigens. ISBT Newslett No 18, April 1983. 4 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. 5 Lewis M: The Working Party on Terminology for Red Cell Surface Antigens. ISBT Newslett No 34, April 1987. 6 Race RR, Sanger R: Blood Groups in Man, ed 6. Oxford, Blackwell, 1975. 7 Issitt PD: Applied Blood Group Serology, ed 3. Miami, Montgomery Scientific Publications, 1985. 8 Shows TB, McAlpine PJ, Boucheix C, et al: Guidelines for human gene nomenclature. Human Gene Mapping 9, Paris 1987. Cytogenet Cell Genet 1987;46:11-28. 9 Sistonen P, Nevanlinna H, Virtaranta-Knowles K, et al: Ne”, a new blood group antigen in Finland. Vox Sang 1981;40:352. 10 Sistonen P, Tippett P: A ‘new’ allele giving futher insight into the LW blood group system. Vox Sang 1982;42:252. 11 Sistonen P: Linkage of the LW blood group locus with the complement C3 and Lutheran blood group loci. Ann Hum Genet 1984;48;239. 12 Giles CM: ‘Partial inhibition’ of anti-Rg and anti-Ch reagents. 11. Demonstration of separable antibodies for different specificities. Vox Sang 1985;48:167. 13 Giles CM: Three Chido determinants detected on BSRg+ allotype of human C4: their expression in Ch-typed donors and families. Hum Immunol1987;18:111. 14 Giles CM, Jones J W A new antigenic determinant for C4 of relatively low frequency. Immunogenetics 1987;26:392. 15 Salmon Ch, Cartron J-P, Rouger Ph: The Human Blood Groups. Paris, Masson, 1984. 16 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. 17 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. 18 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. 19 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. 20 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. 21 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. ISBT/ICSH Working Party 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. Immunology 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: Decayaccelerating 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 Aunfrom the loci for Kell and Colton blood group systems. Transfusion (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 (Phila) 1975;15:270. 35 Fellous M, Hors MC, Rebourcet R, et al: The expression and relation of HLA, µglobulin 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. 165 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 recommends that ‘blood groupers’ continue to use the conventional symbol MNS. 015 (Colton). The CO locus has been linked to the argininosuccinate 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 replacement 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, Overbeeke 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 testing ‘new’ antigen with antibody specific for numbered antigen. For high-incidence antigen: Column C: indicate + or - for result of testing cells of ‘new’ antibody producer 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 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 Proposed name A B A C KEL2 RH29 - - - - __ - - - - RH34 - - KEL13 MNS5 MNS28 MNS2Y RH17 RH18 ~ - KEL4 KEL5 KEL7 KELll KEL12 + or - for Incidence B C - - - - - - - - __ - __ - - _ . A B C A - - 206.1 - - CWRG3 - - CWRG4 - - CWRG5 - - __ CWRG6 - - __ CWRGll__ __ 206.2 CWRGl CWRG2 - 207.1 207.2 208.1 209.1 209.3 B C - - ~ __ ~ - - __ - __ __ __ __ __ __ __ 168 ISBT/ICSH Working Party Appendix 3 cont. RH44 KEL14 CWRG12 RH46 KEL16 H1 RH47 KEL18 XKl LU2 KEL19 201.2 LU3 KEL20 201.3 LU4 KEL22 201.4 - LU5 FY3 202.1 - 901.6 LU6 N 5 202.2 - 901.7 LU7 JK3 202.5 901.8 LU8 D12 202.6 Lull YT1 202.7 - LU12 sc1 202.9 901.11 LU13 sc3 202.10 - LU16 co1 203.2 901.13 LU17 C03 205.1 LW5 205.3 - LW6 205.4 205.6 205.7 Investigator: D. Application for ISBT Number. + :- offspring Inheritance: ratio + :- siblings 901.4 901.5 901.9 901.10 901.12 - Inclusion in a collection: collection name Genetic: Biochemical: E. Aii . B. Exclusion from blood group systems: List systems and z counts' for each List substitute markers and z counts for each Pertinent-serum available for: in-house testing Pertinent cells available for: in-house testing Investigator: Inclusion in a system: system name ,circulation , circulation 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. Genetic: give lods at e = 0.00' Serological: give details (e.g. altered expression of other antigens in system) ' Biochemical: 901.3 Serological: Proposed Symbol Ai . Inheritance: ratio C. 901.2 Date: Appendix 4 Proposed Name 901.1 Consult Race and Sanger [6, pp. 552-5591 for determination. ISBT/ICSH Working Party 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 591660 Dr. G. W. G. Bird: Regional Blood Transfusion Centre, Vincent Drive, Edgbaston, Birmingham B13 9XH, UK Dr. E. Brodheim: Columbia University, Dept. of Industrial Engineering 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 Stephenson 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. FAX 045-6 78 40 16 Dr. L. Kornstad: Statens Institute for Folkeshelse, Dept. of Immunology, 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 169 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 Centre, 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 952019973, USA Mr. J. J. Moulds: Gamma Biologicals Inc., 3700 Mangum Rd., Houston, TX 77092, USA. FAX (713) 956 3333 Prof. Dr. H. R. Nevanlinna: Finnish Red Cross Blood Transfusion Service, Kivihaantie 7, SF-00310, Helsinki 31, Finland. FAX 5801329 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 Sanguines. CNTS St Antoine, 53, boulevard Diderot, 75571 Paris Cedex 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, Kivihaantie 7, SF-00310, Helsinki 31, Finland. FAX 5801329 Dr. P. Tippett: MRCBlood Group Unit, Wolfson House, 4 Stephenson Way, London NW12HE, UK. FAX 01-3882374 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 Service, 301 Pine St., Adelaide 5000, Australia. FAX 08-2237280