Tissue Antigens (1975), 6,80-84 Published by Munksgaard, Copenhagen, Denmark No part may be reproduced by any process without written permission from the author(s)
HL-A Phenotyping in an Indonesian Population M. ABDULSALAM~, J. G O N Y M. ~ , SCHMID~, H. DASTOT~, M. R E B O U LJ. ~ ,H O R S L. ~ , D E G O S ~CH. , SOLAL~, 1 AND J. COL0MBANI2 A. H. MARKUM of Hematology, Department of Childhealth, Medical School, University of Indonesia, Jakarta, Indonesia; and 2 Laboratoire d'Immuno-HBmatologie, INSERM U93, HGpital Saint-Louis, Paris, France
1 Division
The frequencies of 30 HL-A antigens were studied in an Indonesian population of 95 individuals from the city of Jakarta. The antigens HL-AS, or more precisely W24, and HL-A1 1 (first series) and W15 (second series) occurred with high frequencies, whereas HL-A8, W14 and W22 were completely absent. These results are consistent with previous reports of HL-A typing in South East Asian populations.
Received for publication 7 June, accepted 9 September 1974
The genetic relationship between various ethnic groups using the H G A system as a genetic marker have been studied many times. A number of observations indicate that each ethnic group possesses its oswn characteristic HL-A antigenic profile (Dausset et al. 1965, Albert et al. 1970, Morris et al. 1971, Kissmeyer-Nielsen & Thorsby 1970, Colombani & Degos 1972, Bodmer et al. 1972). Certain antigens such as HL-A1 and HL-A8 occur mostly in Caucasian populations, while H G A 9 is more common in non-Caucasian ethnic groups. The purpose of this paper is to present our investigation of the HL-A phenotypes of 95 unrelated individuals from the city of Jakarta, the capital of Indonesia. The re-
sults were compared with those of Engelfriet et al. (1972) in the South Moluccans, the inhabitants of the Eastern part of the Indonesian archipelago, and with the HL-A phenotypes of populations from other parts of South East Asia. Materials and Methods This investigation was carried out on 87 unrelated, healthy volunteers, the medical personnel from the Department of Childhealth, Medical School, University of Indonesia, Jakarta, and on eight unrelated Indonesian students staying in Paris. Most of them (76.8 %) originated from Java Island, in the southern part of the Indonesian archipelago.
Supported in part by Contracts 72-7-0489 and 72-7-005 from the D.G.R.S.T. and A 9293 from the N.I.H. and by a scholarship from the Centre International des Stages (Ministhe des Affaires Etrangsres), Paris, France.
81
HL-A PHENOTYPING IN AN INDONESIAN POPULATION
Blood samples were collected in heparinized tubes and in EDTA tubes within two months. Those obtained from the donors in Jakarta were sent by air to Paris. Owing to the geographical distance between Jakarta and Paris ( 11,700 km) , HL-A typing was performed between 36 and 48 h after the blood was collected. Lymphocytes were separated from heparinized blood by Ficoll-Isopaque (Harris & Ukaejiofo 1970) and were typed using Terasaki’s two-stage lymphocytotoxicity test (Mittal et al. 1968) at 37’ C using unabsorbed rabbit complement; and platelets from EDTA blood were typed using the platelet complement fixation method (Colombani et al. 1971) . The 120 antisera used for this study were obtained from this laboratory. I n all cases, blood was typed for the following H G A specificities: First locus: HL-A1, 2, 3, 9, 10 (W25, W26), 11, W28, W29, W32, Da25 (W30 +31). Second locus: HGA5, 7, 8, 12, 13, W5, W10, W14, W15, W17, W18, W21, W22, W27, Da31 (part of W16 - Dausset et al. 1972). In 73 cases out of 95, the subdivision of HL-A9 into W23 and W24 was also defined. All cases were tested using the platelet complement fixation technique for the broad specificity W19 using serum Duvilliers (W19+HGAl, 3, 11) and serum Rohrig (W19i-HL-A 10). The HL-A nomenclature used was as defined in the Fifth International Histocompatibility Workshop. All cases were also tested for TY, a new specificity determined at the second locus (Gelsthorpe & Doughty 1973). Gene frequency was calculated according to the following formula: P = 1 where f is the frequency of positive
vm,
individuals, and by maximum likelihood. The linkage disequilibrium or was estimated according to Mattiuz et al.’s equation (1970) :
a=i/j- pmm n
n
n
where a, b, c and d are the number of the f f , --, - 4- and -- phenotypes, and n the total number of individuals. Haplotype frequencies were computed by the formula Pij = PiPj A,where Pi and Pj are the frequencies of the genes i and j studied (computed by the maximum likelihood). In this way, some negative haplotype frequency values occur where a negative value is high. I n such cases, the haplottype frequency must be considered to be virtually zero.
+
+
Results and Discussion Good reliability was observed between the two techniques performed in parallel. However, in some cases the lymphocytes were in poor Condition (more than 20 % background dead cells). In these cases the platelet complement fixation test was repeated in order to confirm the specificities observed. I n all cases the platelets were in fairly good condition. As mentioned above, all cases were tested against a serum containing anti-Wl9, HL-A1, 3, 11 (Duvilliers) and one containing anti-W19 and anti-HL-A10 (Rohrig) using platelet complement fixation. Fourteen cases out of 95 were reactive with these sera, but did not react with antLW29, anti-Da25 ( = W30 f W31), anti-W32, anti-HGAl, 3, 10 and 11 in either technique. It is possible that these individuals possess a special subgroup of W19, referred to as W19X in Table 1. In as much as none of them were tested against anti-Fe55, which is considered part of the W19 complex (Ferrara et al. 1973),
82
ABDULSALAM E T AL.
Table 1 Antigen and gene frequencies Antigens tested First locus
Phenotype frequency
HL-A1 HL-A2 HL-A3 HL-A11 HL-A9* W25 W26 W28 W29 W32 Da25 W19X Blank
6.32 32.63 1.05 40.00 57.89 0.00 5.26 2.11 1.05 2.11 6.32 14.74
Yo
-
Gene
frequency (Maximum likelihood)
Standard deviation
0.0315 0.1700 0.0052 0.2263 0.3566"' 0.0000 0.0263 0.0105 0.0000 0.01 11 0.0329 0.0329 0.0451
0.0127 0.0279 0.0052 0.031 3 0.0365
0.0974 0.0257 0.0000 0.0463 0.0429 0.0789 0.0707 0.0000 0.3086 0.0472 0.1190 0.0051 0.0000 0.0257 0.0103 0.0103 0.0000 0.1127
0.0116 0.0074 0.0076 0.0130 0.0204 0.0256
South Malays Moluccans (H.T. 72 p. 651) ( H . T . 72 p. 651)
.oo .12
.oo .06 .54
.oo
.03 .15 .02 .16 .40
.oo
.03
.oo
.01 .01
.oo
.02
.16 .09
.20*""
0.0217 0.0114
.04 .02
.06 .05
0.0152 0.0146 0.0196 0.0186
.02 .01 .25 .08
.03 .08 .10 .05
0.0352 0.01 54 0.0238 0.0051
.19
.29 .06 ND ND .03 .02 ND .05 ND .18
Second locus
HL-A5 HL-A7 HL-A8 HL-A12 HL-A13 w5 w10 W14 w15 W17 W18 w21 w22 W27 TY Da31 Da30 Blank
16.84 5.16 0.00 9.47 8.42 15.79 13.69 0.00 53.68 9.47 21.05 1.05 0.00 4.21 1.05 2.11 0.00 -
0.0114 0.0072 0.0072 0.0282
.oo
.oo
.oo .08
.oo .01 .06 ND
.oo
ND .24
.oo
.oo
(Gene frequencies of South Moluccans typed by Engelfriet et al. 1972 and of Malays by Joysey et al. 1972). The blank values indicate the frequency of unknown genes. * Of which 18.60% were W23 and 81.40% W24. *' Maximum likelihood: W23: 0.051236; W24: 0.29847. *** Gene Malay (Histocompatibility Testing 1972, p. 253) is included under blank.
the possibility of this antigen being present can not yet be excluded. A new antigen, also considered to be a subdivision of W19, known as antigen Malay (Bodmer et al.
1972) was independently described by Joysey et al. (1972), Payne et al. (1972a,b) and Morris et al. (1971) in South East Asia. These individuals reacted with one
83
HL-A PHENOTYPING I N AN INDONESIAN POPULATION
or more of the following First Internatio- ilar as far as HL-A gene frequencies are nal Histocompatibility Workshop lympho- concerned, these three populations are very cytotoxic sera: 69 Li, 32 and 83. These different from other South East Asian popsera recognise the part of the W19 group ulations: HL-A5 and W10 are less frewhich is not W29, W30, W31 or W32. Se- quent; W24 is more frequent. I t is possible to separate these popularum Rohrig also recognises part of W19 which is not W29, W30, W31 or W32. Ac- tions completely from those of Oceania cordingly, it is possible that the Malay and Australia, since W22 is very rare or antigen is present in the Indonesian pop- even absent in Indonesia, whereas it has a very high frequency in Australia and Oceulation. In the total population, the frequency of ania (.02 to .44). Conversely, W5 and HLH L A 9 was 57.89 %, with W24 predomi- A5 are absent from Australia and Oceania, nating (81.4 % of HL-AS) (Table 1j. but are present in Indonesia. Computations of the haplotype frequenOther high frequency antigens were W 15 (53.68 %) and HL-A11 (40 %). HL-A8, cies and linkage disequilibrium values W14 and W22 were completely absent, show that the most frequent haplotype is and HL-Al, 3, 10 and W28 (first locus) HL-AS, W15 (0.0938). The highest posivalues are HL-AS, W18 (0.0342), and H G A 7 , 12, 13, W17, W21, W27 and tive Da31 (second locus) were found to be of H L A 9 , W5 (0.0332), HL-A2, W10 (0.0255) (Table 2). low frequency. With the exception of HLThe haplotype HL-AS, W15 is frequent A l l and W5, these findings were almost identical to those of Engelfriet et al. ( 1972) in Mongoloids from South East Asia and in the South Moluccans, the inhabitants of in Indonesians. Nevertheless, in most of value is negative the eastern part of the Indonesian archi- these populati'ons the pelago. I n this study, the frequency of W5 (Indonesians, South Moluccans, Malaywas lower than that found in the South sians, Sherpas, Filipinos, Chinese, Ainus). value for HL-AS, W5 was Moluccans, and HL-A1 1 occurred with A positive higher frequency. I n comparison with the also found in Malays and South MolucHL-A phenotypes of other South-East cans. Although a positive value for HLAsian populations, this investigation also concurs with Joysey et al.'s (1972) results A2, W10 is not found in South Moluccans or Malays, it is found in Japanese and among the Malayan population. However, although the Indonesians, Koreans. Finally the disequilibrium HL-AS, W 18 South Moluccans and Malaysians are sim-
a
Table 2 High
A values in Indonesian popidation compared
to Ma& and South Moluccan populations
HL-A9 W5 Indonesians Malaysians South Moluccans
.033 .069
.059
I
HL-A9 W18 .034 ? ?
I
HL-A2 W10 .025 - ,004
-.010
I
HL-A9 W15
--.016 - .006 -.045
Malay & South Moluccan populations reported in Histocompatibility Testing 1972 by Bodmer et al. in the Joint Report.
84
ABDULSALAM ET AL.
appears to be confined to this sample. Is this due to chance or is it a special feature of this population?
Acknowledgements We should like to express our appreciation to Prof. Dausset for encouraging us to perform this study. We are most grateful to all the laboratory personnel for their assistance, without which this work would not have been possible. We should also like to thank the volunteer blood donors.
References Albert, E. D., Mickey, M. R., McNicholas, A. C. & Terasaki, P. I. (1970) Seven new HL-A specificities and their distribution in three races. Histocompatibility Testing 1970, p. 221 -230. Munksgaard, Copenhagen. Bodmer, J. G., Rocques, P., Bodmer, W. F., Colombani, J., Degos, L. & Dausset, J. (1972) Joint report of the Fifth International Histocompatibility Workshop. Histocompatibility Testing 1972, p. 618-719. Munksgaard, Copenhagen. Colombani, J., D’Amaro, J., Gabb, B., Smith, G. & Svejgaard, A. (1971) International agreement on a microtechnique of platelet complement fixation. Transplant. Proc. 3, 121-126. Colombani, J. & Degos, L. (1972) Variations of HL-A antigens in populations. A survey. Rev. franc. Etud. biol. 27, 551-563. Dausset, J., Ivanyi, P. & Ivanyi, D. (1965) Tissue alloantigens in humans: Identification of a complex system (Hu-1 ). Histocompatibility Testing 1965, p. 51-62. Munksgaard, Copenhagen. Dausset, J., Colombani, J., Legrand, L., Lepage, V., Marcelli-Barge, A. & Dehay, C. (1972) Population and family studies in a French population with special reference to non-HL-A antibodies. Histocompatibility Testing 1972, p. 107-1 16. Munksgaard, Copenhagen. Engelfriet, C. P., van den Berg-Loonen, P. M., van Loghem, E., Nijenhuis, L. E., Veenhovenvon Riesz, L. E. & Kort-Bakker, M. (1972) HL-A and other genetic markers in South Moluccans. Histocompatibility Testing 1972, p. 261-266. Munksgaard, Copenhagen.
Ferrara, G. B., Tosi, R. M., Azzolina, G. & Carminati, G. (1973) A new HL-A antigen a t the H G A locus positively associated with the W14 (Maki) specificity of the FOUR locus. Tissue Antigens 3, 130-135. Gelsthorpe, K. & Doughty, R. W. (1973) A new HL-A antigen, Ty. Tissue Antigens 3, 3 16-3 22. Harris, R. & Ukaejiofo, E. 0. (1970) Tissue typing using a routine one-step lymphocyte separation procedure. Brit. J . Hematology, 18, 229. Joysey, V. C., Roger, J. H., Abbas Amir, Bland, C., Bolton, M., Chan, Duraisamy, G., Jones, A., Joysey, K. A., Lopez, C. G., Megat, B. A. R., Moorcraft, M., Simon, M., Simonsen, M., Subramanian & Wilkinson, M. (1972) Study of a Malay population. Histocompatibility Testing 1972, p. 251-260. Munksgaard, Copenhagen. Kissmeyer-Nielsen, F. & Thorsby, E. (1970) Human transplantation antigens. Transplant. Rev. 4, 109-1 11. Douglas, K. S., Perkins, H. A., Cochrum, K. & Mattiuz, P. L., Ihde, D., Piazza, A., Ceppellini, R. & Bodmer, W. F. (1970) New approaches to the population genetics and segregation analysis of the HL-A system. Histocompatibility Testing 1970, p. 193-205. Munksgaard, Copenhagen. Mittal, K. K., Mickey, M. R., Singal, D. P. & Terasaki, P. I. (1968) Refinement of microdroplet lymphocyte cytotoxicity test. Transplantation 6, 913. Morris, P. J., Ting, A., Alpers, M. P. & Simons, M. (1971) Leucocyte antigens in a New Guinea population. Tissue Antigens 1, 49-52. Payne, R., Kidd, K. K., Radvany, R. & Perkins, H. A. (1972a) HL-A and other polymorphisms of the Chinese of the Canton area. Histocompatibility Testing 1972, p. 197-201. Munksgaard, Copenhagen. Payne, R., Kidd, K. K., Rodvany, R. & Perkins, H. A. (1972b) HL-A and other polymorphisms of the Philipino people. Histocompatibility Testing 1972, p. 203-208. Munksgaard, Copenhagen. Address : M . Abdulsalam Division of Haematology Dept. of Childhealth Medical School University of Indonesia Jakarta, Indonesia
HL-A Phenotyping in an Indonesian Population M. ABDULSALAM~, J. G O N Y M. ~ , SCHMID~, H. DASTOT~, M. R E B O U LJ. ~ ,H O R S L. ~ , D E G O S ~CH. , SOLAL~, 1 AND J. COL0MBANI2 A. H. MARKUM of Hematology, Department of Childhealth, Medical School, University of Indonesia, Jakarta, Indonesia; and 2 Laboratoire d'Immuno-HBmatologie, INSERM U93, HGpital Saint-Louis, Paris, France
1 Division
The frequencies of 30 HL-A antigens were studied in an Indonesian population of 95 individuals from the city of Jakarta. The antigens HL-AS, or more precisely W24, and HL-A1 1 (first series) and W15 (second series) occurred with high frequencies, whereas HL-A8, W14 and W22 were completely absent. These results are consistent with previous reports of HL-A typing in South East Asian populations.
Received for publication 7 June, accepted 9 September 1974
The genetic relationship between various ethnic groups using the H G A system as a genetic marker have been studied many times. A number of observations indicate that each ethnic group possesses its oswn characteristic HL-A antigenic profile (Dausset et al. 1965, Albert et al. 1970, Morris et al. 1971, Kissmeyer-Nielsen & Thorsby 1970, Colombani & Degos 1972, Bodmer et al. 1972). Certain antigens such as HL-A1 and HL-A8 occur mostly in Caucasian populations, while H G A 9 is more common in non-Caucasian ethnic groups. The purpose of this paper is to present our investigation of the HL-A phenotypes of 95 unrelated individuals from the city of Jakarta, the capital of Indonesia. The re-
sults were compared with those of Engelfriet et al. (1972) in the South Moluccans, the inhabitants of the Eastern part of the Indonesian archipelago, and with the HL-A phenotypes of populations from other parts of South East Asia. Materials and Methods This investigation was carried out on 87 unrelated, healthy volunteers, the medical personnel from the Department of Childhealth, Medical School, University of Indonesia, Jakarta, and on eight unrelated Indonesian students staying in Paris. Most of them (76.8 %) originated from Java Island, in the southern part of the Indonesian archipelago.
Supported in part by Contracts 72-7-0489 and 72-7-005 from the D.G.R.S.T. and A 9293 from the N.I.H. and by a scholarship from the Centre International des Stages (Ministhe des Affaires Etrangsres), Paris, France.
81
HL-A PHENOTYPING IN AN INDONESIAN POPULATION
Blood samples were collected in heparinized tubes and in EDTA tubes within two months. Those obtained from the donors in Jakarta were sent by air to Paris. Owing to the geographical distance between Jakarta and Paris ( 11,700 km) , HL-A typing was performed between 36 and 48 h after the blood was collected. Lymphocytes were separated from heparinized blood by Ficoll-Isopaque (Harris & Ukaejiofo 1970) and were typed using Terasaki’s two-stage lymphocytotoxicity test (Mittal et al. 1968) at 37’ C using unabsorbed rabbit complement; and platelets from EDTA blood were typed using the platelet complement fixation method (Colombani et al. 1971) . The 120 antisera used for this study were obtained from this laboratory. I n all cases, blood was typed for the following H G A specificities: First locus: HL-A1, 2, 3, 9, 10 (W25, W26), 11, W28, W29, W32, Da25 (W30 +31). Second locus: HGA5, 7, 8, 12, 13, W5, W10, W14, W15, W17, W18, W21, W22, W27, Da31 (part of W16 - Dausset et al. 1972). In 73 cases out of 95, the subdivision of HL-A9 into W23 and W24 was also defined. All cases were tested using the platelet complement fixation technique for the broad specificity W19 using serum Duvilliers (W19+HGAl, 3, 11) and serum Rohrig (W19i-HL-A 10). The HL-A nomenclature used was as defined in the Fifth International Histocompatibility Workshop. All cases were also tested for TY, a new specificity determined at the second locus (Gelsthorpe & Doughty 1973). Gene frequency was calculated according to the following formula: P = 1 where f is the frequency of positive
vm,
individuals, and by maximum likelihood. The linkage disequilibrium or was estimated according to Mattiuz et al.’s equation (1970) :
a=i/j- pmm n
n
n
where a, b, c and d are the number of the f f , --, - 4- and -- phenotypes, and n the total number of individuals. Haplotype frequencies were computed by the formula Pij = PiPj A,where Pi and Pj are the frequencies of the genes i and j studied (computed by the maximum likelihood). In this way, some negative haplotype frequency values occur where a negative value is high. I n such cases, the haplottype frequency must be considered to be virtually zero.
+
+
Results and Discussion Good reliability was observed between the two techniques performed in parallel. However, in some cases the lymphocytes were in poor Condition (more than 20 % background dead cells). In these cases the platelet complement fixation test was repeated in order to confirm the specificities observed. I n all cases the platelets were in fairly good condition. As mentioned above, all cases were tested against a serum containing anti-Wl9, HL-A1, 3, 11 (Duvilliers) and one containing anti-W19 and anti-HL-A10 (Rohrig) using platelet complement fixation. Fourteen cases out of 95 were reactive with these sera, but did not react with antLW29, anti-Da25 ( = W30 f W31), anti-W32, anti-HGAl, 3, 10 and 11 in either technique. It is possible that these individuals possess a special subgroup of W19, referred to as W19X in Table 1. In as much as none of them were tested against anti-Fe55, which is considered part of the W19 complex (Ferrara et al. 1973),
82
ABDULSALAM E T AL.
Table 1 Antigen and gene frequencies Antigens tested First locus
Phenotype frequency
HL-A1 HL-A2 HL-A3 HL-A11 HL-A9* W25 W26 W28 W29 W32 Da25 W19X Blank
6.32 32.63 1.05 40.00 57.89 0.00 5.26 2.11 1.05 2.11 6.32 14.74
Yo
-
Gene
frequency (Maximum likelihood)
Standard deviation
0.0315 0.1700 0.0052 0.2263 0.3566"' 0.0000 0.0263 0.0105 0.0000 0.01 11 0.0329 0.0329 0.0451
0.0127 0.0279 0.0052 0.031 3 0.0365
0.0974 0.0257 0.0000 0.0463 0.0429 0.0789 0.0707 0.0000 0.3086 0.0472 0.1190 0.0051 0.0000 0.0257 0.0103 0.0103 0.0000 0.1127
0.0116 0.0074 0.0076 0.0130 0.0204 0.0256
South Malays Moluccans (H.T. 72 p. 651) ( H . T . 72 p. 651)
.oo .12
.oo .06 .54
.oo
.03 .15 .02 .16 .40
.oo
.03
.oo
.01 .01
.oo
.02
.16 .09
.20*""
0.0217 0.0114
.04 .02
.06 .05
0.0152 0.0146 0.0196 0.0186
.02 .01 .25 .08
.03 .08 .10 .05
0.0352 0.01 54 0.0238 0.0051
.19
.29 .06 ND ND .03 .02 ND .05 ND .18
Second locus
HL-A5 HL-A7 HL-A8 HL-A12 HL-A13 w5 w10 W14 w15 W17 W18 w21 w22 W27 TY Da31 Da30 Blank
16.84 5.16 0.00 9.47 8.42 15.79 13.69 0.00 53.68 9.47 21.05 1.05 0.00 4.21 1.05 2.11 0.00 -
0.0114 0.0072 0.0072 0.0282
.oo
.oo
.oo .08
.oo .01 .06 ND
.oo
ND .24
.oo
.oo
(Gene frequencies of South Moluccans typed by Engelfriet et al. 1972 and of Malays by Joysey et al. 1972). The blank values indicate the frequency of unknown genes. * Of which 18.60% were W23 and 81.40% W24. *' Maximum likelihood: W23: 0.051236; W24: 0.29847. *** Gene Malay (Histocompatibility Testing 1972, p. 253) is included under blank.
the possibility of this antigen being present can not yet be excluded. A new antigen, also considered to be a subdivision of W19, known as antigen Malay (Bodmer et al.
1972) was independently described by Joysey et al. (1972), Payne et al. (1972a,b) and Morris et al. (1971) in South East Asia. These individuals reacted with one
83
HL-A PHENOTYPING I N AN INDONESIAN POPULATION
or more of the following First Internatio- ilar as far as HL-A gene frequencies are nal Histocompatibility Workshop lympho- concerned, these three populations are very cytotoxic sera: 69 Li, 32 and 83. These different from other South East Asian popsera recognise the part of the W19 group ulations: HL-A5 and W10 are less frewhich is not W29, W30, W31 or W32. Se- quent; W24 is more frequent. I t is possible to separate these popularum Rohrig also recognises part of W19 which is not W29, W30, W31 or W32. Ac- tions completely from those of Oceania cordingly, it is possible that the Malay and Australia, since W22 is very rare or antigen is present in the Indonesian pop- even absent in Indonesia, whereas it has a very high frequency in Australia and Oceulation. In the total population, the frequency of ania (.02 to .44). Conversely, W5 and HLH L A 9 was 57.89 %, with W24 predomi- A5 are absent from Australia and Oceania, nating (81.4 % of HL-AS) (Table 1j. but are present in Indonesia. Computations of the haplotype frequenOther high frequency antigens were W 15 (53.68 %) and HL-A11 (40 %). HL-A8, cies and linkage disequilibrium values W14 and W22 were completely absent, show that the most frequent haplotype is and HL-Al, 3, 10 and W28 (first locus) HL-AS, W15 (0.0938). The highest posivalues are HL-AS, W18 (0.0342), and H G A 7 , 12, 13, W17, W21, W27 and tive Da31 (second locus) were found to be of H L A 9 , W5 (0.0332), HL-A2, W10 (0.0255) (Table 2). low frequency. With the exception of HLThe haplotype HL-AS, W15 is frequent A l l and W5, these findings were almost identical to those of Engelfriet et al. ( 1972) in Mongoloids from South East Asia and in the South Moluccans, the inhabitants of in Indonesians. Nevertheless, in most of value is negative the eastern part of the Indonesian archi- these populati'ons the pelago. I n this study, the frequency of W5 (Indonesians, South Moluccans, Malaywas lower than that found in the South sians, Sherpas, Filipinos, Chinese, Ainus). value for HL-AS, W5 was Moluccans, and HL-A1 1 occurred with A positive higher frequency. I n comparison with the also found in Malays and South MolucHL-A phenotypes of other South-East cans. Although a positive value for HLAsian populations, this investigation also concurs with Joysey et al.'s (1972) results A2, W10 is not found in South Moluccans or Malays, it is found in Japanese and among the Malayan population. However, although the Indonesians, Koreans. Finally the disequilibrium HL-AS, W 18 South Moluccans and Malaysians are sim-
a
Table 2 High
A values in Indonesian popidation compared
to Ma& and South Moluccan populations
HL-A9 W5 Indonesians Malaysians South Moluccans
.033 .069
.059
I
HL-A9 W18 .034 ? ?
I
HL-A2 W10 .025 - ,004
-.010
I
HL-A9 W15
--.016 - .006 -.045
Malay & South Moluccan populations reported in Histocompatibility Testing 1972 by Bodmer et al. in the Joint Report.
84
ABDULSALAM ET AL.
appears to be confined to this sample. Is this due to chance or is it a special feature of this population?
Acknowledgements We should like to express our appreciation to Prof. Dausset for encouraging us to perform this study. We are most grateful to all the laboratory personnel for their assistance, without which this work would not have been possible. We should also like to thank the volunteer blood donors.
References Albert, E. D., Mickey, M. R., McNicholas, A. C. & Terasaki, P. I. (1970) Seven new HL-A specificities and their distribution in three races. Histocompatibility Testing 1970, p. 221 -230. Munksgaard, Copenhagen. Bodmer, J. G., Rocques, P., Bodmer, W. F., Colombani, J., Degos, L. & Dausset, J. (1972) Joint report of the Fifth International Histocompatibility Workshop. Histocompatibility Testing 1972, p. 618-719. Munksgaard, Copenhagen. Colombani, J., D’Amaro, J., Gabb, B., Smith, G. & Svejgaard, A. (1971) International agreement on a microtechnique of platelet complement fixation. Transplant. Proc. 3, 121-126. Colombani, J. & Degos, L. (1972) Variations of HL-A antigens in populations. A survey. Rev. franc. Etud. biol. 27, 551-563. Dausset, J., Ivanyi, P. & Ivanyi, D. (1965) Tissue alloantigens in humans: Identification of a complex system (Hu-1 ). Histocompatibility Testing 1965, p. 51-62. Munksgaard, Copenhagen. Dausset, J., Colombani, J., Legrand, L., Lepage, V., Marcelli-Barge, A. & Dehay, C. (1972) Population and family studies in a French population with special reference to non-HL-A antibodies. Histocompatibility Testing 1972, p. 107-1 16. Munksgaard, Copenhagen. Engelfriet, C. P., van den Berg-Loonen, P. M., van Loghem, E., Nijenhuis, L. E., Veenhovenvon Riesz, L. E. & Kort-Bakker, M. (1972) HL-A and other genetic markers in South Moluccans. Histocompatibility Testing 1972, p. 261-266. Munksgaard, Copenhagen.
Ferrara, G. B., Tosi, R. M., Azzolina, G. & Carminati, G. (1973) A new HL-A antigen a t the H G A locus positively associated with the W14 (Maki) specificity of the FOUR locus. Tissue Antigens 3, 130-135. Gelsthorpe, K. & Doughty, R. W. (1973) A new HL-A antigen, Ty. Tissue Antigens 3, 3 16-3 22. Harris, R. & Ukaejiofo, E. 0. (1970) Tissue typing using a routine one-step lymphocyte separation procedure. Brit. J . Hematology, 18, 229. Joysey, V. C., Roger, J. H., Abbas Amir, Bland, C., Bolton, M., Chan, Duraisamy, G., Jones, A., Joysey, K. A., Lopez, C. G., Megat, B. A. R., Moorcraft, M., Simon, M., Simonsen, M., Subramanian & Wilkinson, M. (1972) Study of a Malay population. Histocompatibility Testing 1972, p. 251-260. Munksgaard, Copenhagen. Kissmeyer-Nielsen, F. & Thorsby, E. (1970) Human transplantation antigens. Transplant. Rev. 4, 109-1 11. Douglas, K. S., Perkins, H. A., Cochrum, K. & Mattiuz, P. L., Ihde, D., Piazza, A., Ceppellini, R. & Bodmer, W. F. (1970) New approaches to the population genetics and segregation analysis of the HL-A system. Histocompatibility Testing 1970, p. 193-205. Munksgaard, Copenhagen. Mittal, K. K., Mickey, M. R., Singal, D. P. & Terasaki, P. I. (1968) Refinement of microdroplet lymphocyte cytotoxicity test. Transplantation 6, 913. Morris, P. J., Ting, A., Alpers, M. P. & Simons, M. (1971) Leucocyte antigens in a New Guinea population. Tissue Antigens 1, 49-52. Payne, R., Kidd, K. K., Radvany, R. & Perkins, H. A. (1972a) HL-A and other polymorphisms of the Chinese of the Canton area. Histocompatibility Testing 1972, p. 197-201. Munksgaard, Copenhagen. Payne, R., Kidd, K. K., Rodvany, R. & Perkins, H. A. (1972b) HL-A and other polymorphisms of the Philipino people. Histocompatibility Testing 1972, p. 203-208. Munksgaard, Copenhagen. Address : M . Abdulsalam Division of Haematology Dept. of Childhealth Medical School University of Indonesia Jakarta, Indonesia
