Download Blood Group Terminology 1990 - International Society of Blood

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, &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.
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