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T Akaza

Publications and source records attributed to T Akaza.

At least 91 records · Page 5Linked to original sources

Two subtypes of HLA-B51 differing by substitution at position 171 of the alpha 2 helix.

Newly defined antigens of the B5, B35 cross-reacting group have been found in Japanese and North American Indians. Nucleotide sequencing of the alleles encoding the Japanese B5.35 antigen and the variant B5 antigen from the Piman Indians show them to be identical. This new allele, B*5102, differs from B*5101 by a single nucleotide substitution that changes residue 171 from histidine to tyrosine. Residue 171, which is part of the alpha 2 helix, is believed to contribute directly to peptide interaction in the A pocket of the binding groove and is either histidine or tyrosine in all HLA-A, B, C heavy chains. Tyrosine 171 is shared by B*5102, B*3501, B*3502, and B*5301 and must be responsible for the serological cross-reactivities of these molecules not shared with B*5101. Stimulation of lymphocytes from a B*5101 positive donor with B*5102 positive cells failed to generate cytotoxic T cells with specificity for the difference between these molecules. However, one out of five clones of cytotoxic T cells raised against B*5101 failed to lyse targets expressing B*5102. Substitution of histidine for tyrosine at residue 171 affected recognition of HLA-B35-restricted human minor histocompatibility antigen-specific T cell clones.

Amino Acid Sequence↗

Family study on HLA-DPB1 polymorphism: linkage analysis with HLA-DR/DQ and two "new" alleles.

An extensive family study on HLA-DPB1 was performed in 105 families living in northeastern Japan. In a linkage study between HLA-DPB1 and other HLA loci, five apparent recombinations between DPB1 and DR/DQ loci were observed. The recombination frequency (theta) with maximum probability was estimated to be 0.017 by the lod score method. DPB1 allele and haplotype frequencies in unrelated parents were determined by direct counting. The most common allele was DPB1*0501 with the frequency of 41.2% and the second was DPB1*0201 with 24.0%. Nine DPB1-DR and six DPB1-DQ haplotypes were in significant linkage disequilibrium. Seven kinds of extended haplotypes were observed to be over 1%, in which the most common haplotype A24-B52-DR15-DQ6-DPB1*0901 occurred at 6.0%. Moreover, we found two "new" DPB1 alleles in this study. The first one possesses a single base substitution from DPB1*0501 resulting in an amino acid change. The other is most likely to be formed by an intraexonic recombination between DPB1*0301 and DPB1*0501.

Alleles↗

Anti-idiotypic antibody to T-cell receptor in multiply transfused patients may play a role in resistance to graft-versus-host disease.

Most patients who receive multiple blood or platelet transfusions do not develop graft-versus-host disease (GVHD) in spite of the transfusion of donor white cells--cells that are capable of engraftment and subsequent GVHD. The object of this study was to search for the factors responsible for resistance to GVHD in such patients. Some sera from patients who have received multiple platelet transfusions inhibit the proliferation of alloreactive T-cell clones that function as an in vitro model of donor-derived proliferating T cells recognizing recipient alloantigens. The humoral factor in such sera was capable of binding to the T-cell clones, but not to stimulator cells. Further analysis revealed that the humoral factor in such sera was IgG, which specifically bound to membrane molecules of the T-cell clones. The antibody competed with WT31, a monoclonal antibody (MoAb) to T-cell receptor (TCR), in binding to TCR of the T-cell clones. It did not compete with CD3 or CD2 MoAb. These observations strongly favor the view that the antibody against TCR exists in the sera of multiple transfusion recipients. It is suggested that the TCR antibody binds to TCR of the T-cell clones, thus blocking the interaction of the T-cell clone with alloantigens of stimulator cells and resulting in inhibition of the proliferation of T-cell clones. Furthermore, in view of T-cell clone-specific binding of the antibody in sera, it might be concluded that the antibody is anti-idiotypic.

Antibodies, Anti-Idiotypic↗

No evidence for linkage between the loci for coagulation factor XIII-A and HLA.

The linkage analysis between the locus for coagulation factor XIII-A (F13A) and HLA region genes (HLA-A, -C, -B) was performed. In males, the maximum of lod scores between F13A and HLA was 0.33 at 0 = 0.30, and in females lod scores were negative at all values of 0. The results provided no evidence for close linkage between F13A and HLA genes.

Chromosome Mapping↗

Haplotype study on C4 polymorphism in Japanese. Associations with MHC alleles, complotypes, and HLA-complement haplotypes.

Genetic polymorphism of the fourth component of human complement (C4) was investigated in 83 Japanese families which have been typed for HLA-A,-B,-C,-DR, C2, and BF. Four common C4A alleles and four common C4B alleles were observed. The allele frequencies estimated from unrelated parents were as follows: C4A3, 0.686; A4, 0.132; A2, 0.106; AQ0, 0.067; ARares, 0.009; C4B1, 0.587; B2, 0.167; B5, 0.088; and BQ0, 0.158. Eight different C4 haplotypes were observed with frequencies of more than 0.01. The estimated haplotype frequencies were as follows: C4A3-B1, 0.513; A4-B2, 0.114; A2-BQ0, 0.106; A3-B5, 0.088; AQ0-B1, 0.059; A3-BQ0, 0.047; A3-B2, 0.038; A4-B1, 0.015; and Rares, 0.021. Strong positive gametic associations were found in the following C4-HLA haplotypes: C4A2BQ0-A24, C4A2BQ0-Bw52, C4A3B5-Bw54, C4A3B5-Bw59, C4A4B2-Bw46, C4A3B5-Cw1, C4A2BQ0-DR2, and C4A3B5-DR4. Eleven complotypes were observed with frequencies of more than 0.01. C4A2BQ0 and C4A3B5 were exclusively associated with BFS-C2C. BFF was associated with C4A3B1. C2AT, C2B, and C2BH were associated with C4A3B1, A4B2, and C4A3B1, respectively. Eight different HLA-complement haplotypes were found to be characteristic of Japanese. These combinations are considerably different from those reported in Caucasoid populations.

Alleles↗

HLA antigens in patients with unexplained hepatitis following halothane anesthesia.

We examined HLA-A,B,C and DR locus antigens in 38 Japanese patients who had recovered from halothane hepatitis. The patients were divided into two subgroups, i.e. jaundice and non-jaundice groups, because the clinical features were quite different in each. DR2 was positive in 14 (58.3%) of 24 patients with jaundice, compared with 281 (33.6%) of the 837 Japanese healthy controls (chi-square with Yates' correction = 5.30, relative risk = 2.77, P less than 0.025). Conversely, Bw44 was increased in non-jaundice patients (50.0%), compared with 157 (12.7%) of the 1234 Japanese healthy controls (chi-square with Yates' correction = 13.75, relative risk = 6.86, P less than 0.001). The haplotype frequency (Hf) of Aw24-Bw52-DR2 was high in the patients with jaundice (Hf = 0.2362), while it was zero in the patients without jaundice (P less than 0.0042). These data suggest that the two groups of halothane hepatitis have different genetic backgrounds.

Adolescent↗

HLA antigens and adult T-cell leukemia virus infection: a community-based study in the Goto Islands, Japan.

In order to study the genetical susceptibility to infection by adult T-cell leukemia virus (ATLV), which is considered to be a main causative agent of adult T-cell leukemia (ATL), the HLA profile of persons with antibody against ATLV-associated antigen (anti-ATLA) was compared with that of antibody-negative persons in villages A and B of the Goto Islands, a typical ATL endemic area in Kyushu, Japan. The frequency (29%) of HLA-B7 in persons with anti-ATLA was significantly higher than that (8%) in anti-ATLA negatives (corrected X2 = 7.73, p less than 0.01) in one village while the frequency of HLA-B7 was around 10% in both positive and negative persons in the other village. These results do not support or deny the possibility of the existence of individuals who are genetically susceptible to ATLV infection in ATL endemic areas of Japan.

Adult↗

[HLA and cervical carcinoma (author's transl)].

For the purpose of studying immunogenetic factors related to disease susceptibility to cervical carcinoma (squamous cell carcinoma), HLA-A,B and DR typings were performed by the standard microlymphocytotoxicity test using about 240 typing antisera in 66 Japanese patients with cervical carcinoma and 206 healthy individuals. The results obtained were as follows: 1) The patients had a significant association with HLA-Bw46 (gene frequency = 6.3%, relative risk = 3.9, p less than 0.025), compared with the controls (g.f. = 1.7%). 2) The patients had a significant association with HLA-DRw8 (g.f. = 17.3%, r.r. = 2.3, p less than 0.05), compared with the controls (g.f. = 8.9%). 3) When the patients with cervical carcinoma were divided into two groups, i.e. 53 patients with invasive carcinoma of the cervix and 13 patients with carcinoma in situ of the cervix, the former had a more significant association with both HLA-Bw46 (g.f. = 6.8%, r.r. = 4.3) and HLA-DRW8 (g.f. = 19.2%, r.r. = 2.6) than the total patients, compared with the controls. However, the latter showed only a negligible association when compared with the controls. 4) The significant linkage disequilibrium between HLA-Bw46 and HLA-DRw8 was found in the patients with cervical carcinoma (haplotype frequency = 0.059, delta = 0.047, p less than 0.002), but not in the controls (h.f. = 0.0097, delta = 0.0075). 5) On the other hand, the significant linkage disequilibrium between HLA-A2 and HLA-Bw46 was found in both the patients and the controls.

Carcinoma, Squamous Cell↗

Both HLA-DR restricted and nonrestricted functions of adherent cells are required for induction of T lymphocyte proliferative responses.

There appeared to be two distinct functions of adherent cells in human T lymphocyte proliferative responses to purified protein derivative (PPD). The first is antigen-presenting ability which is mediated by antigen-presenting cells (APC) among adherent cells. By employing antiserum blocking pretreatment of APC, it was revealed that HLA-DR antigens are involved in this function and that identity or partial identity of HLA-DR antigens between APC and T lymphocytes is required for T lymphocyte antigen recognition. The second function is mediated by the soluble factor produced by adherent cells and is HLA-DR nonrestricted. Although it remains unclear whether APC and adherent cells producing the soluble factor belong to the same cell population, this second function might lead T lymphocytes to proliferative as long as T lymphocytes recognize antigen (PPD) via APC.

Animals↗

Human antigen-presenting cells: characterization of the cells in the T-lymphocytes proliferative response.

Human antigen-presenting cells (APC) which present the antigen to T lymphocytes resulting in a T-lymphocyte proliferative response were found among peripheral mononuclear cells (MNC), by employing purified protein derivative (PPD) as soluble antigen. To assess the adherence capacity of human antigen-presenting cells, MNC were separated by plastic Petri dishes or nylon wool columns. Plastic nonadherent cells were almost equivalent to unseparated cells in antigen-presenting ability. Plastic adherent cells, however, showed better antigen-presenting ability than unseparated cells. On the other hand, cells passed over nylon wool columns showed essentially no ability to present PPD to T lymphocytes. Removal of phagocytic cells by carbonyl iron resulted in about 50-70% reduction in antigen-presenting ability. Carrageenan, which is known to be toxic to macrophages, had no effect on APC. By using both rabbit anti-human Ia-like antiserum and alloantiserum specific for HLA-DR phenotype and complement, it was shown that APC possessed Ia-like antigens, whereas they did not bear surface immunoglobulins. These results indicate that the human APC is probably a cell in the monocyte-macrophage lineage. Allogeneic MNC were used as APC in order to determine whether any genetic restriction exists between MNC as APC and responding T lymphocytes. Optimal stimulation was shown to require identity of mixed leukocyte reaction (MLR)- activating determinants between APC and T lymphocytes. It is however, obscure whether an HLA-D region restriction exists in these combinations because PPD-pulsed allogeneic MNC lost their ability to elicit even MLR. It is possible that this failure to elicit MLR was caused by T lymphocytes among the MNC used as APC.

Antigens↗