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At least 19 recordsLinked to original sources
PubMed1991

HLA-DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 genes in Japanese multiple sclerosis patients.

Japanese MS patients and controls were examined for the distribution of HLA-DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 alleles using in vitro amplification of genomic DNA and probing with sequence-specific oligonucleotides. No significant difference in frequency of the examined alleles was observed among the two groups. This is in contrast to Norwegian MS patients, where an association to a combination of certain DQA1 and DQB1 alleles has previously been demonstrated.

Alleles↗
PubMed1992

Linkage disequilibrium between DPA1 and DPB1 alleles among Norwegian Caucasoids and Japanese.

Associations between alleles at the DPA1 and DPB1 loci were analyzed in 181 Norwegian caucasoids. Associations were observed between the DPA1*0201 and the DPB1*0101, *0901, *1001 and *1101 alleles. An association between DPA1*0201 and the DPB1*0901 allele was also observed among 23 healthy Japanese and 24 Japanese MS patients. In addition, it appeared that among Japanese the DPA1*0201 allele may be associated to the DPB1*0501. In conclusion, alleles at the DPA1 and DPB1 loci display different associations among Norwegian caucasoids and Japanese.

Alleles↗
PubMed1991

HLA class II nucleotide sequences, 1991.

The HLA class II sequences included in this compilation are taken from publications listed in the accompanying paper, Nomenclature for factors of the HLA system, 1990 (Bodmer et al., 1991), and Nomenclature for factors of the HLA system, 1989 (Bodmer et al., 1990). Where discrepancies have arisen between reported sequences the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments identity between residues is indicated by a hyphen (-). An unavailable sequence is indicated by an asterisk (*). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid number.

Base Sequence↗
PubMedDate not supplied

DNA polymorphism of HLA class II genes in alopecia areata.

We investigated the DNA restriction polymorphism (RFLP) of the Major Histocompatibility Complex (MHC) class II genes: HLA-DQA, -DQB, -DPA, and -DPB in 20 Danish patients with alopecia areata (AA) and in healthy Danes. The frequency in AA of the DQB1*0301 and DQw7 associated DQB Bgl/II 4.2 kb fragment was increased to 65.0 per cent compared to 23.2 per cent in controls (RR = 6.1; p less than 10(-3)) suggesting that the previously reported associations between AA and both DR4 and DR5 is secondary to an association between AA and DQB1*0301, which codes for the beta-chain of the HLA-DQ molecule of the serologically defined HLA-DQw7 specificity. Individuals who carried both DQA1*0501 and DQB1*0301 seemed to have a further increased risk of developing AA compared to individuals carrying only one of these HLA class II genes. Analysis of the combined presence of DQB1*0301 and DPA1*0103 in AA suggests that an additive risk effect (synergism or interaction) exists between the DQB1*0301 and DPA1*0103 alleles which are situated at different HLA class II loci.

Alopecia Areata↗
PubMed1992

Interferon-gamma response region in the promoter of the class II MHC gene, DPA.

The class II MHC gene DPA is inducible by interferon-gamma (IFN-gamma), whereas the DQB gene is not inducible in most cell types. To investigate the DNA region specifically responsible for inducibility or its lack that may be required (in addition to the elements required for constitutive expression of class II genes), hybrid promoters were constructed between the proximal 5' regions of the DPA promoter up to -148 bp, which is IFN-gamma inducible, and of the DQB promoter up to -160 bp, which is not inducible. As a result of these and previous studies [9, 10], the region of the DPA gene required for its IFN-gamma inducibility was localized to 27 bp between -55 and -81, including the Y-box element and its flanking nucleotides.

Base Sequence↗
PubMed1992

Sequencing and population analysis of four novel HLA-DPA1 alleles.

We determined the base sequences of the HLA-DPA1 gene from four B-lymphoblastoid cell lines (CB6B, LKT3, AMAI, and T7526) that showed distinct electrophoretic patterns of single-stranded polymerase chain reaction products of the HLA-DPA1 gene. The novel HLA-DPA1 alleles of CB6B, LKT3, AMAI, and T7526 were designated DPA1*02021, DPA1*02022, DPA1*0301, and DPA1*0401, respectively. Although there was only one base substitution between DPA1*02021 and DPA1*02022, the single-strand conformation polymorphism of these two alleles was clearly demonstrated by electrophoresis in a nondenaturing polyacrylamide gel containing 10% glycerol. In addition, we genotyped for the HLA-DPA1 gene of healthy unrelated Oriental individuals--i.e., 227 Japanese, 88 Papua New Guineans, and 41 Buyi-Chinese--to demonstrate the ethnic distribution of the HLA-DPA1 alleles.

Alleles↗
PubMed1991

Construction of intertypic chimeric dengue viruses by substitution of structural protein genes.

Dengue virus contains an 11-kilobase positive-strand RNA genome that codes for, in one open reading frame, three structural proteins (capsid, premembrane, and envelope), followed by seven nonstructural proteins. The structural protein genes of a full-length cDNA clone of type 4 dengue virus were replaced with the corresponding genes of dengue 1 or dengue 2 to create intertypic chimeric cDNA. The RNA transcripts made from these templates were infectious when transfected into permissive cells in culture. Progeny of chimeric cDNA produced apparently authentic dengue 1 or dengue 2 structural proteins, together with dengue 4 nonstructural proteins, and as a consequence exhibited type 1 or type 2 serological specificity. Both of the chimeras ultimately grew to the same titer as their type 1 or type 2 parent, but the type 2/type 4 chimera grew very slowly. This chimera also produced small plaques; in contrast, the type 1/type 4 chimera produced normal size plaques. The type 2/type 4 chimera retained the mouse neurovirulence of the dengue 2 virus, which was the source of its structural protein genes. Each of the mice inoculated intracerebrally with the chimera died, but survival time was prolonged. The retardation of replication of the type 2/type 4 chimeric virus suggests that this virus and possibly other intertypic dengue virus chimeras with similar properties should be examined for attenuation in primates and possible usefulness in a live dengue virus vaccine for humans.

Animals↗