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T Amano

Publications and source records attributed to T Amano.

At least 361 records · Page 20Linked to original sources
PubMed1981

Idiotypic analysis of antibodies to hen egg-white lysozyme (HEL). III. Further studies on the idiotypic cross-reactivity among anti-HEL antibodies in mice.

An isolated antibody preparation directed to the native hen egg-white lysozyme (HEL) from a single A/J mouse (#a-11), termed IDHELa-11, was inoculated into rabbits to produce anti-idiotypic sera (anti-Id). The antisera were extensively absorbed with normal A/J Ig to render then idiotype specific. Radioimmunoassay utilizing 125I-IdHELa-11 and the anti-ID sera (R103 and R104) was performed to examine the idiotypic cross-reactivity of the humoral immune response to HEL in various mouse strains and other animal species. Idiotypes shared by IdHELa-11 were detected in the sera of five mouse strains tested, but not in any of the examined sera of other animal species such as rats, goats, guinea pigs, or sheep, indicating the occurrence of species-specific cross-reactive idiotypes (CRI) of antibodies to HEL. Our experiments also suggested the presence of intrastrain CRI. The present experiments, along with our earlier results (15), suggest that idiotypic cross-reactivity among murine antibodies to HEL appears to be weak. Thus when R103 and R104 were the anti-Id sera used, the frequency of occurrence of CRI shared by IdHELa-11 in 5 micrograms of anti-HEL antibody in strain A mice was 74 ng and 111 ng; in other strains it was 25-44 ng and 60-98 ng, respectively.

Animals↗
PubMed1981

Suppression of hen egg-white lysozyme (HEL)- specific delayed -type hypersensitivity responses in mice by suppressor T cells after neonatal administration of anti-idiotypic antibodies.

Anti-idiotypic rabbit antiserum (anti-Id) directed to the idiotypes of anti-hen egg-white lysozyme (HEL) antibody froma single C3H mouse (No. 2) was shown to be capable of recognizing only a fraction of the anti-HEL antibody populations produced by other C3H mice. Experiments were performed to examine the effect of this particular anti-Id on the delayed-type hypersensitivity (DTH) response specific for the same protein antigen. A group of 60-day-old C3H mice which had been administered anti-Id within 24 hr after birth were tested for HEL-DTH response. The results indicated that the DTH response was completely suppressed by the anit-Id treatment. The inhibition of DTH reactivity is due to active suppression and involves the generation of suppressor T cells. Thus, the suppression induced with a single injection of anti-Id was transferable with both spleen cells and thymocytes from mice, that received anti-Id. These suppressor cells are T cells since their ability to suppress DTH is completely abrogated by treatment in vitro with anti-Thy 1.2 serum and complement.

Animals↗
PubMed1981

Subunit structure of alpha-bungarotoxin binding component in mouse brain.

The alpha-bungarotoxin binding component in mouse brain was purified by affinity chromatography with toxin-Sepharose, gel-chromatography on Sepharose 6B, and ion-exchange chromatography with DE52 resin. The iodinated product of the last step produced one major and one minor band on sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). The molecular weight of the minor peak was twice as large as that of the major one. The iodinated product could bind alpha-bungarotoxin, and this binding was inhibited by a nicotinic antagonist, d-tubocurarine, which demonstrated that the iodinated product was a true alpha-bungarotoxin binding component. The molecular structure of the product was analysed by cross-linking followed by SDS-PAGE. The results fitted the model for an alpha-bungarotoxin binding component in the mouse brain composed of six identical or very similar subunits of 51,000--52,000. One subunit carrying the binding site for toxin bound one molecule of toxin. This subunit structure of an alpha-bungarotoxin binding component in the brain is discussed in comparison with that of a nicotinic acetylcholine receptor in the electric organ.

Animals↗
PubMed1981

An immunological determinant for helper T cells at the N- and C-region of hen egg-white lysozyme.

The carrier determinant in the N- and C-region of hen egg-white lysozyme (lysozyme), recognized by T cells, which helps antibody formation to a single DNP residue bound to the Lysine-33 of lysozyme, was analysed. P17 (sequence 1--27: Cys 6-Cys 127: 123--129) and P17t (sequence 1-Homoser 12: Cys 6-Cys 127: 123--129), which are known to be immunodominant antigenic determinants could induce helper T cells. When P17t was reduced and alkylated, one of the resultant peptides, P17tN (sequence 1-Homoser 12) could still induce helper T cells, but P17tC (sequence 123--129) could not. A synthetic peptide SP1-14 (sequence 1-Ala 6--14) also induced helper T cells. Thus the carrier determinant helping in antibody formation to the DNP residue at Lysine-33 may be localized in the region corresponding to the sequence 1--12 of lysozyme.

Amino Acid Sequence↗
PubMed1981

Further studies on complementation between mutants of Clostridium perfringens.

1. Mutants devoid of lambda- and kappa-toxin and hemagglutinin (HA), respectively, were isolated from Cl. perfringens PB6K. The lambda- and HA- mutants could be classified into a and b groups by complementation but the kappa- mutants were all of the a group. 2. All b group mutants isolated, irrespective of the marker used for isolation, were pleiotropically negative or leaky with respect to theta-, lambda- and kappa-toxin and HA production. 3. Lambda-toxin produced by complementation was proved to be a rennet-like protease. 4. The activities of 12 extracellular enzymes, including sialidase, of several b group strains and the parent PB6K were compared, but no definite differences were observed. From this finding, the productions of these enzymes were concluded not to be regulated by the same mechanism as theta-, lambda- and kappa-toxin and HA. 5. Cl. perfringens CN3870 was also studied. Findings were similar to those on PB6K except for very low activity of HA.

Bacterial Toxins↗
PubMed1981

Complementation characteristics of newly isolated mutants from two groups of strains of Clostridium perfringens.

1. Mutants of a group were converted to b group by a second NG treatment. The resulting b group mutants could not produce the marker products that had been lost on the first NG treatment but could produce the others by complementation. 2. Mutants of b group were converted to constitutive mutants by a second NG treatment. No back mutation from b group was observed.

Bacterial Toxins↗
PubMed1981

Presence and location of an O-acetyl group in O4-antigen of Vibrio parahaemolyticus.

A polysaccharide moiety (PS) released from O4-LPS of Vibrio parahaemolyticus was purified. The constituent sugars of the purified PS were glucose, galactose, arabinose, fucose, heptose, N-acetyl galactosamine and an unknown N-acetyl amino sugar. The unknown amino sugar was deduced to be a terminal deoxy amino sugar from its NMR spectrum. PNMR spectroscopy at 200 MHz, periodate oxidation and treatment with alpha-L-fucosidase of the purified PS sample before and after alcoholic sodium methoxide-treatment suggested that PS contained an O-acetyl and alpha-linked non-reducing terminal L-fucose and that the O-acetyl group was located at the C-2 or C-4 position of the non-reducing terminal fucose. The contribution of the O-acetyl group located in L-fucose to the O4-antigenic determinant seemed to be small, judging from immunochemical experiments.

Acetylation↗
PubMed1981

Idiotypic analysis of antibodies to hen egg-white lysozyme (HEL). II. Distribution and frequency of occurrence of idiotypes shared by A/J anti-HEL antibody.

Anti-HEL Ab from one A/J mouse (No. a-4),Ida-4(HEL), was s.c. inoculated into rabbits to induce anti-idiotypic (anti-Id) sera. After absorption with normal A/J Ig, two anti-Id serra (R101 and R102) were obtained. The interaction between 125I-Id(a-4)(HEL) and anti-Id sera was completely inhibited by unlabelled Ida-4(HEL), but not by non-specific Ig. The anti-Id sera were used to investigate the distribution of A/J (No. a-4) anti-HEL idiotypes in sera obtained from HEL-immunized animals. Idiotypes shared by Ida-4(HEL) were also detected in the sera of five examined mouse strains, but not in any of the examined rat, guinea-pig, goat, and sheep sear. Our experiments suggest the presence of inter- as well as intrastrain idiotype in mice. However, cross-reactivity appeared to be weak. When R101 and R102, respectively, were the anti-Id sera used, the frequency of occurrence of Ida-4(HEL) in stain A wa 1/106 and 1/53; in other mouse strains it was 1/277 and 1/85.

Animals↗
PubMed1980

Effects of nimodipine (Bay e 9736) on cerebral circulation in cats.

The response of feline pial arteries to i.v. administration of isopropyl-(2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate (nimodipine, Bay e 9736) was studied by means of the vidicon camera system developed in our laboratory. Pial arteries showed a dose-dependent dilation with a reduction of systemic arterial blood pressure in the dose range of 0.001 mg/kg to 0.1 mg/kg of nimodipine. The dilatory response was more marked in the smaller arteries (< 100 mu) than in the larger ones (greater than or equal to 100 mu).

Animals↗