DNA TYPING FOR CLASS-II HLA ANTIGENS WITH ALLELE-SPECIFIC OR GROUP-SPECIFIC AMPLIFICATION .5. TYPING FOR SUBSETS OF HLA-DR1 AND DR'BR'

被引:25
作者
GAO, XJ [1 ]
MORAES, JR [1 ]
MILLER, S [1 ]
STASTNY, P [1 ]
机构
[1] UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED,5323 HARRY HINES BLVD,DALLAS,TX 75235
关键词
D O I
10.1016/0198-8859(91)90084-M
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Three DRB1 alleles of the DR1 group including DRB1*0101, DRB1*0102, and DRB1*0103 are currently recognized. The first two of these are defined as HLA-DR1 by serologic typing and as either Dw1 or Dw20 by typing with T cells. DRB1*0103, previously called DR'Br' or DR'BON', is not detectable by serology. Little information exists about the population frequencies of DRB1*0102 and DRB1*0103. In the present study we have used the polymerase chain reaction (PCR) and allele-specific oligonucleotide probes to determine these alleles. To avoid cross-hybridization with other DRB genes having the same DNA sequences as those of the region to be analyzed, we performed group-specific PCR to amplify only DR1 DRB1 genes. This was accomplished using a 21-nucleotide-long primer, homologous to the first hypervariable region common to the DR1 DRB1 genes, and which under appropriate conditions amplified only DRB1 genes of the DR1 group. Five oligonucleotide probes, one matching the second hypervariable region, two spanning the third hypervariable region, and two covering codons 82 through 89, were used to determine the three alleles. DRB1*0101 (Dw1) was found to be the major type of DR1 in North American Caucasians. In North American black and Brazilian mestizo populations DRB1*0102 (Dw20) was more prevalent. DRB1*0103 (DR'Br') was detected in only six individuals in the present study.
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页码:147 / 154
页数:8
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共 21 条
  • [1] HLA ANTIGENS AND SERONEGATIVE RHEUMATOID-ARTHRITIS
    BARDIN, T
    LEGRAND, L
    NAVEAU, B
    MARCELLIBARGE, A
    DEBEYRE, N
    LATHROP, GM
    POIRIER, JC
    SCHMID, M
    RYCKEWAERT, A
    DRYLL, A
    [J]. ANNALS OF THE RHEUMATIC DISEASES, 1985, 44 (01) : 50 - 53
  • [2] BIDWELL L, 1988, HUM IMMUNOL, V26, P191
  • [3] NOMENCLATURE FOR FACTORS OF THE HLA SYSTEM, 1989
    BODMER, JG
    MARSH, SGE
    PARHAM, P
    ERLICH, HA
    ALBERT, E
    BODMER, WF
    DUPONT, B
    MACH, B
    MAYR, WR
    SASAZUKI, T
    SCHREUDER, GMT
    STROMINGER, JL
    SVEJGAARD, A
    TERASAKI, PI
    [J]. TISSUE ANTIGENS, 1990, 35 (01): : 1 - 8
  • [4] BRAUTBAR C, 1986, TISSUE ANTIGENS, V28, P8
  • [5] CAMBONTHOMSEN A, 1986, TISSUE ANTIGENS, V27, P256
  • [6] COPPIN HL, 1990, J IMMUNOL, V144, P984
  • [7] ECKELS D, 1989, IMMUNOBIOLOGY HLA, V1, P502
  • [8] INVOLVEMENT OF CLASS-II BETA-CHAIN AMINO-ACID RESIDUE-85 AND RESIDUE-86 IN T-CELL ALLORECOGNITION
    ECKELS, DD
    GEIGER, MJ
    SELL, TW
    GORSKI, JA
    [J]. HUMAN IMMUNOLOGY, 1990, 27 (03) : 240 - 253
  • [9] DNA TYPING FOR CLASS-II HLA ANTIGENS WITH ALLELE-SPECIFIC OR GROUP-SPECIFIC AMPLIFICATION .2. TYPING FOR ALLELES OF THE DRW52-ASSOCIATED GROUP
    FERNANDEZVINA, M
    SHUMWAY, W
    STASTNY, P
    [J]. HUMAN IMMUNOLOGY, 1990, 28 (01) : 51 - 64
  • [10] HLA-DR4 SUBSETS IN PATIENTS WITH TYPE-I DIABETES - A STUDY BY DOT BLOT HYBRIDIZATION WITH SYNTHETIC OLIGOMERS AND AMPLIFIED HLA-DR GENOMIC DNA
    GAO, X
    BALL, EJ
    HOOVER, M
    CAPRA, JD
    STASTNY, P
    [J]. HUMAN IMMUNOLOGY, 1988, 23 (02) : 97 - 97