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T Akaza

Publications and source records attributed to T Akaza.

At least 73 records · Page 4Linked to original sources
PubMed1995

Both HLA-B*1301 and B*1302 exist in Asian populations and are associated with different haplotypes.

A B13 split antigen was newly identified with three alloantisera in Japanese, and two B13 split antigens were found in a Thai family. To confirm the variation of B13 and understand the correspondence between the serologic splits and the published B13 alleles, B*1301 and B*1302, we determined the sequences of genes coding for these B13 splits. The common Japanese B13 allele was found to be B*1301, whereas another split antigen was shown to be coded by B*1302. Two B13 variants identified in a Thai individual corresponded to B*1301 and B*1302. Moreover, 57 B13-positive samples from several ethnic groups were examined using the PCR-SSO method. Differing from previous reports, both B*1301 and B*1302 were found in samples from Asian populations. These two alleles were separately associated with different antigens: HLA-B*1301 exhibited a strong association with A2, Cw10, DR12, and DQ7 antigens, whereas HLA-B*1302 was strongly associated with A30, Cw6, DR7, and DQ2 antigens. In addition, applying the PCR-SSCP method, B*1301 and B*1302 could also be simply distinguished from each other.

Alleles↗
PubMed1995

A new HLA-C allele, Cw*1403, associated with HLA-B44 in Japanese.

An allele encoding an HLA-C antigen, tentatively called CX44, associated with HLA-B44 was identified as a new member of the Cw14 group, Cw*1403. The nucleotide sequence of Cw*1403 was closest to that of Cw*1401: five bases were different between the two alleles, in which three bases in Cw*1403 (two in exon 3 and one in exon 4) were the same as those of most HLA-C alleles. Two substitutions from guanine to adenine were found in the new allele, both of which are in exon 2, one at position 134 (61 of exon 2) and the other at position 201 (128 of exon 2). The former nucleotide substitution leads to the substitution of amino acid residue 21 from Arg to His, and the other substitution was synonymous. The former substitution was shared with Cw2, 3, 5, 13, and 15 alleles, and the latter was shared with Cw2, 4, 5, 8, 12, 13, 15 and 16 alleles. The other seven unrelated Japanese samples with CX44 were analyzed by a PCR-SSO method. It was confirmed that all the seven samples have the same substitutions as the sequenced allele, and the allele demonstrates a strong association with A33, B44, DR13, and DQ1, which are known to form a common haplotype in Japanese and Koreans.

Alleles↗
PubMed1995

Distribution of HLA antigens and haplotypes in the Buryat population of Siberia.

Polymorphisms of HLA-A, B, C, DR, and DQ antigens were investigated in a Mongoloid population named Buryat living in Siberia. HLA gene and haplotype frequencies were calculated from the population data obtained from 141 unrelated healthy Buryat adults. Gene frequencies of class I antigens A2, A24, A1, B61, Cw10, and Cw6 were estimated to be more than 10%. For class II, DR4, DR7, DR13, DQ7, and DQ1 antigens were predominant. A phylogenetic tree was constructed based on HLA gene frequencies, and the Buryat population was clustered with the Mongoloid groups in Northeast Asia. In the analysis of HLA-A, C, B, DR, and DQ five-locus haplotype frequencies, seven kinds of haplotypes were calculated to occur at frequencies of more than 2%. Five of the seven common haplotypes have also been described in the other human populations thus far. Some of the haplotypes have been described in European populations, while the others were shared with Northeast Asian Mongoloids as well as Amerindians. Similar situation was also found in the analysis of class I (HLA-A, C, B) three locus haplotypes. These observations suggest the unique genetic background of this Buryat population.

Ethnicity↗
PubMed1995

DNA-based typing of human platelet antigen systems by polymerase chain reaction-single-strand conformation polymorphism method.

Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) method has been established to discriminate genotypes for the human platelet antigen (HPA) systems HPA-1, HPA-2, HPA-3, HPA-4, and HPA-5. Gene fragments which contain polymorphic sequences corresponding to the HPA-1, HPA-2, HPA-3, HPA-4, and HPA-5 systems were PCR-amplified with specific primers. The amplified DNA was denatured and subjected to non-denaturing polyacrylamide gel electrophoresis followed by silver staining. The results obtained by the PCR-SSCP method were in good agreement with those of the allotypes determined by serological typing. Furthermore, the results agreed with those obtained by other DNA-based typing methods such as PCR-allele-specific restriction enzyme analysis and PCR-sequence-specific primer. These results indicate that PCR-SSCP is a simple and sensitive method for determining HPA genotypes and identifying unknown polymorphisms.

Antigens, Human Platelet↗
PubMed1995

Multiplex ARMS-PCR-RFLP method for high-resolution typing of HLA-DRB1.

A reliable method for high-resolution HLA-DRB1 typing using the combination of group-specific amplification and RFLP analysis is described. Group-specific PCR amplification (multiplex ARMS-PCR) was carried out under the same conditions for all groups using seven different primer pairs divided into four groups: (1) DR1 and DR10; (2) DR2, DR7 and DR9; (3) DR3 DR5, DR6 and DR8, and (4) DR4. The subsequent polyacrylamide gel electrophoresis was used to determine the group(s) contained in each sample. DR1, DR2/7, DR3/5/6/8, DR4, DRB1*0901 and DRB1*1001 could be distinguished easily using this system. Computer analysis of the various restriction enzyme cleavage sites was carried out on 105 DRB1 allele sequences. It was shown that all DRB1 alleles, except for five allele pairs and some alleles possessing silent mutations, could be distinguished with commonly available restriction endonucleases. Computer analyses on the discrimination of the heterozygous and homozygous combinations were also carried out. Although some heterozygous combinations could no be distinguished with single digestion, double digestion using two restriction enzymes could distinguish most of such heterozygotes. The results of the typing of 100 Japanese individuals using this method showed good agreement with those obtained by other methods.

Alleles↗
PubMed1994

Analysis of risk factors for post-transfusion graft-versus-host disease in Japan. Japanese Red Cross PT-GVHD Study Group.

We distributed a questionnaire to highlight the effects of post transfusion graft-versus-host disease (PT-GVHD) and to elucidate the risk factors that would predispose people to the disease. The questionnaire described the pathogenesis and the clinical profiles of PT-GVHD and was distributed to doctors in Japan whose hospital conducted more than 1000 units of blood transfusions a year. Doctors were asked about their awareness and experience of PT-GVHD cases. Those who had seen cases of PT-GVHD were then asked to detail clinical course and laboratory data. Of the 14,083 doctors who replied to the first question, 47.4% did not realise that PT-GVHD could occur in immunocompetent hosts. From 304 cases where detailed information was supplied, 171 were considered clinically compatible with PT-GVHD. From these it seems that the risk factors linked to PT-GVHD are cardiovascular surgery, cancer, fresh and consanguineous blood transfusion, and being male. Patients with any of these factors should have some prophylactic therapy such as irradiation of blood before transfusion.

Adolescent↗
PubMed1994

Alloreactive feature of HLA-DP-specific cytotoxic T-cell clone.

The alloreactive feature of CD4+ cytotoxic T-cell clone that could specifically lyse the cells bearing DPB1*0202 sequence was described. The clone was generated from a mixed culture of peripheral blood lymphocytes derived from siblings who were HLA-A, B, C, DR, and DQ identical by serological typing and whose DNA sequence of the second exon of DPB1 was one-allele mismatched by oligonucleotide typing (responder, PDB1*0201/0402; stimulator, DPB1*0202/0402). Specific cytotoxic activity of the clone was strictly limited against the cells bearing DPB1*0202 and was not able to lyse the other tested cells bearing DPB1*0201, 0301, 0401, 0501, 0601, 0901, 1301, and 1601. The cytotoxic activity of the clone was blocked by treatment of target cells with anti-DP monoclonal antibodies (B7/21). On the other hand, treatment of target cells with blocking agents of endogenous or exogenous antigen transport pathway (brefeldin A (BFA), endogenous; chloroquine, exogenous) had no effect on the cytotoxic activity of the clone. These results strongly favor the view that the DP epitopes recognized by the clone are conformational epitopes conferred by specific amino acids in hypervariable regions of the HLA-DP second DPB1 exon and the contribution of peptides in the HLA grooves to the conformational epitope motif is less likely.

Acyclovir↗
PubMed1994

Effect of single amino acid substitution at residue 167 of HLA-B51 on binding of antibodies and recognition of T cells.

We recently showed that a single amino acid substitution of tryptophane into glycine at residue 167 facing the "A pocket" forms a novel HLA-B51 subtype, B*5103, which is serologically discriminated as HLA-BTA. CDC assay of human alloantisera specific for the HLA-B5 CREG against B*5103- or B*5101-transfected human B-cell line, Hmy2C1R (C1R), supported the belief that human alloantisera can discriminate B*5103 from B*5101 Ag. Moreover, we found that 4D12 anti-B5, B35 CREG mAb cannot bind to B*5103 Ag on C1R cells or L cells although it binds to B*5101 Ag on both cells. These results indicate that alloantibodies can detect a single amino acid substitution at residue 167. Furthermore, it was suggested that 4D12 mAb recognizes the structure formed by the HLA-peptide complex since this mAb did not bind to empty HLA-B5, B35 CREG Ag on RMA-S transfectants. Six of eight anti-HLA-B*5101 CTL clones are not able to kill C1R cells expressing B*5103, indicating that conformational change of the A pocket by substitution at residue 167 has a crucial influence on recognition of alloreactive T cells. Therefore, discrimination of B*5103 from B*5101 would seem to be important in bone marrow transplantation.

Amino Acid Sequence↗
PubMed1994

Sequences of four splits of HLA-A10 group. Implications for serologic cross-reactivities and their evolution.

Nucleotide sequences of alleles encoding four serologically defined splits of the HLA-A10 group, A26.1, A26.3, A26.4, and A10SA, were determined. It was confirmed that the alleles coding for A26.1 and A26.3 are identical with A*2602 and A*2601, respectively. On the other hand, alleles for A26.4 and A10SA are thus far undescribed. A26.4 (A*2603) was different from the other A26 splits at three positions: 74 histidine, 76 valine, and 77 aspartate. A10SA (A*2604) was different from A26.3 (A*2601) by a single substitution of arginine by leucine at position 163. A comparison of amino acid sequences of HLA-A10 cross-reacting antigens revealed that all of the A10 group antigens share specific amino acids: 142 isoleucine, 144 glutamine, 145 arginine, 149 threonine, and 152 glutamate. Moreover, A26.1, A26.3, A10SA, and A43 share 76 alanine and 77 asparagine, which is consistent with the reported serologic cross-reactivity. The close relationship between the alleles for the A10 cross-reacting group was supported by a phylogenetic tree analysis for the HLA-A alleles.

Alleles↗
PubMed1994

Sequence analysis of serological HLA-A11 split antigens, A11.1 and A11.2.

HLA-A11 has two serologically-defined splits, A11.1 and A11.2, and two alleles coding for HLA-A11, A*1101 and A*1102, have been published so far. In order to understand the relationship between the serological subtypes and the amino acid sequences, we have sequenced the alleles coding for A11.1 and A11.2. The results demonstrated that A11.1 split antigen is encoded by A*1101 and A11.2 split antigen is encoded by A*1102. Moreover, we obtained the sequences of exons 1, 5, 6, 7, and 8 of A*1102, which were not reported previously. In addition, we could distinguish A*1101 from A*1102 using a PCR-SSCP method, confirming that A11.1 carried by different HLA haplotypes has the same sequence.

Amino Acid Sequence↗
PubMed1994

Protection against natural killer cells by interferon-gamma treatment of K562 cells cannot be explained by augmented major histocompatibility complex class I expression.

Prior study has revealed that the expression of certain major histocompatibility complex (MHC) class I molecules on the membranes of normal or transformed cells can prevent natural killer (NK)-cell-mediated killing. This has been explained by either (1) the target interference model, or (2) the effector inhibition model. In both cases, MHC class I molecules are concerned but the precise mechanisms are still unclear. The erythroleukaemia K562 cell is known as a NK-sensitive target. This sensitivity has been explained mostly as being due to lack of MHC class I antigens on the K562 membrane. However, several recent studies have indicated that the expression of MHC class I antigens on the cell does not solely explain the protection against NK cells. To elucidate the mechanism of NK-cell-mediated killing, we investigated the killing profiles of the K562 cells by NK cells. Previous studies indicated that the NK-sensitive K562 cells can express some MHC class I antigens on their surface, and become protective against NK-cell killing after treatment with human interferon-gamma (hIFN-gamma). In the present study, we show that this resistance is not rendered by MHC class I expression, because addition of anti-MHC class I monoclonal antibodies (mAb) in the killing assay of hIFN-gamma-treated K562 cells, which express MHC class I antigens as the target, did not restore the sensitivity to NK cells. Moreover, we show that spontaneously occurring K562 clones which could not express MHC class I antigens even after hIFN-gamma treatment, could be protected after treatment with the cytokine. Taken together, these results strongly suggest that the susceptibility of K562 cells to NK cell killing is due to some elements distinct from those related to MHC class I antigens.

Antibodies, Monoclonal↗
PubMed1993

Behçet's disease associated with one of the HLA-B51 subantigens, HLA-B* 5101.

The strong association of Behçet's disease with HLA-B51 in several ethnic groups is well known. Because the HLA-B51 antigen has been recently identified to comprise three alleles, HLA-B* 5101, HLA-B* 5102, and HLA-B* 5103, we sought to investigate whether there is any correlation of one particular allele among them with B51-positive patients with Behçet's disease. Forty-six Japanese patients with Behçet's disease and HLA-B51 were typed by using the alloantisera, which allowed the subdivision of B51 antigen by the microlymphocyte toxicity assay. All the patients were found to carry HLA-B* 5101. This result suggests that amino acid substitutions at residue 167 or 171 prevent the development of Behçet's disease, because HLA-B* 5101 differs from HLA-B* 5102 and HLA-B* 5103 by single amino acid substitution at residues 171 and 167, respectively, or that another non-HLA gene tightly linked to the HLA-B* 5101-associated haplotype around the HLA class I gene region is responsible for the susceptibility to Bechçet's disease. This study provides insight into the molecular mechanism underlying an HLA association with Behçet's disease.

Alleles↗
PubMed1993

Molecular analysis of HLA-B39 subtypes.

Serological studies have suggested the presence of a new HLA-B39 subtype (B39.2) in the Japanese population. To identify the new HLA-B39 subtype and compare it with an other HLA-B39 subtype (B39.1), the genes encoding HLA-B39.1 (B*39013) and B39.2 (B*3902) have been cloned from Japanese. We have sequenced these genes and completed the sequence of HLA-B39.1 (B*39011) gene from a Caucasian that was partially sequenced. Comparison of the sequence data revealed that B*3902 and B*39013 differ by three nucleotide substitutions which result in a two amino acids change at residues 63 and 67, while one silent substitution at codon 312 is found between B*39011 and B*39013. These results suggest that B*3902 has evolved from B*39013 rather than B*39011.

Amino Acid Sequence↗
PubMed1993

Structural analysis of HLA-B40 epitopes.

Two genes encoding HLA-B60 or HLA-B61 were cloned from Japanese and the exons of their genes were sequenced. One silent mutation was observed at the exon 1 between HLA-B60 (B*40012) and B*40011. Seven nucleotide substitutions were seen at the exon 3 between HLA-B61 (B*4006) and B*4002. Three substitutions at codon 95, CTC in B*4002 to TGG in B*4006, changed Leu in B*4002 to Trp in B*4006, while two substitutions at codon 97, AGC in B*4002 and ACG in B*4006, changed Ser in B*4002 to Thr in B*4006. Since B*4002 shares the epitope of alloantibodies specific for HLA-B61, two HLA-B61 subtypes are discriminated by two amino acid substitutions at residues 95 and 97. B*40012 and B*4006 differ by four amino acid substitutions on the beta sheet and five amino acid substitutions on the alpha 2 helix. Since the residues at the beta sheet seem hardly to affect the binding of alloantibody, it is suspected that the residues on the alpha 2 helix provide epitopes for alloantibodies that discriminate allospecificity between HLA-B60 and HLA-B61.

Amino Acid Sequence↗
PubMed1993

Genotyping and association analysis of HLA-B61 in Japanese.

The distribution of HLA-B61-related alleles, B*4002-B*4006, was examined in the Japanese population by using PCR-SSO and PCR-RFLP methods. About half of the B61-positive individuals possessed B*4002 and the remaining half possessed B*4006. In addition, these two major B61 alleles were separately associated with different HLA-C alleles: B*4002 exhibited a strong linkage disequilibrium with Cw10, whereas B*4006 was strongly associated with C blank and DR9. Amino acid residues that contribute to the serologic epitopes of the B61 group and their relationships with other HLA-B locus antigens are discussed.

Alleles↗
PubMed1993

Establishment of human minor histocompatibility antigen-specific cytotoxic T cell clones restricted by HLA-DR9.

Cytotoxic T lymphocyte clones specific for human minor histocompatibility (hmH) antigens were generated in vitro from PBL, of a healthy female donor, which had been repeatedly stimulated with PBL MHC antigens of her healthy, genotypically identical brother (HLA type of the siblings was A11/A2 B35/B62 Cw4/Cw- DR4.2/DR9 DQ3/DQ- DPB1*0102/DPB*0501). Two clones were obtained that had specific killing activity against PBL- or EBV-transformed B cell line (BCL) derived from stimulator, but not from autologous cells. A panel study of the killing patterns of these two clones, using various HLA phenotype BCLs (33 BCLs) generated from healthy donors as targets, revealed that these two clones killed some DR9-bearing BCLs (5 in 20 BCLs), but did not kill the remaining DR9-bearing BCLs (15 in 20 BCLs) or other DR-type BCLs (13 BCLs). Furthermore, the killing activities of these two clones were greatly inhibited by pretreatment of the target stimulator-derived BCL with anti-HLA DR mAb. It was thus concluded that these two clones recognized hmH antigens in HLA DR9 in a restricted manner.

Antibodies, Monoclonal↗