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Biomedical subjects

I Tadokoro

Publications and source records attributed to I Tadokoro.

At least 19 recordsLinked to original sources

4-Hydroxy-3-nitrophenyl (NP) acetyl-hapten specific lymphocyte proliferation. I. Mice bearing Igh-1b allotype can cross-react with 4-hydroxy-5-iodo-3-nitrophenyl (NIP) acetyl hapten.

Hapten specific T cell proliferation was induced in several strains of mice. When lymph node T cells from 4-hydroxy-3-nitrophenyl acetyl-keyhole lympet hemocyanin (NP-KLH)-primed mice were stimulated in vitro with NP-polymer glutamic acid-lysine-phenyl alanine (NP-GL phi) or NP-ovalbumin (NP-OVA), they displayed a good level of proliferative responses. It was observed that NP-GL phi could induce NP-hapten specific proliferation even with NP-KLH lymphocytes from GL phi nonresponder strains. NP-KLH primed lymphocytes from C57BL/6 (H-2b, Igh-1b), CKB (H-2k, Igh-1b), CWB (H-2b, Igh-1b), and B10.BR (H-2k, Igh-1b) mice showed good proliferative responses to both 4-hydroxy-5-iodo-3-nitrophenyl (NIP) acetyl-GL phi and NIP-OVA antigens. However, NP-KLH primed lymphocytes from C3H/He (H-2k, Igh-1j) and C3H. SW (H-2b, Igh-1j) mice displayed poor proliferative responses to NIP-GL phi and NIP-OVA antigen. These results suggested that the gene coding for the NIP-cross-reaction might be mapped in the Ig heavy-chain linked locus.

Animals↗

Genetic control of mouse antibody production to human thyroglobulin.

Genetic control of immune responses in mice against human thyroglobulin was studied using the enzyme-linked immunosorbent assay and passive haemagglutination test. Our results revealed that mice of H-2a, H-2d, H-2q, H-2k and H-2r haplotypes were high responders for antibody production to human thyroglobulin, while mice of H-2b and H-2s haplotypes were low responders. High responsiveness to human thyroglobulin was transmitted to F1 mice in a dominant fashion. Study of the genetic mapping of the immune responses to human thyroglobulin using various congenic mice showed that I-A subregion gene(s) control the immune response to human thyroglobulin.

Animals↗

Genetic control of PQ prolongation of the electrocardiogram in the mouse immunized with the killed group A streptococci.

Genetic control of PQ prolongation of the electrocardiogram (ECG) in the mouse, immunized with killed group A streptococci, was studied by using various congenic mice. Mice of H-2a, H-2k and H-2f haplotypes showed high frequencies of PQ prolongation, while haplotypes of H-2b, H-2d and H-2s showed low frequencies of PQ prolongation. Studies using various recombinant mice revealed that at least one immune-associated (Ir) gene mapped in the left side of the I-B subregion. High responsiveness of F1 hybrids of H-2b and H-2d, as well as B10.A(5R) and B10.A(3R), suggests the existence of a complementing gene. In addition, the differences between C3H and CKB, as well as differences between C3H.SW and CWB, indicate that another Ir gene maps in the immunoglobulin heavy chain (Igh) coding loci. Repeated injections of anti-I-J or anti-I-A antisera also modified this PQ prolongation. These results suggested that both the major histocompatibility complex (MHC) and immunoglobulin (Igh) loci seem to be playing important roles in the pathogenesis of PQ prolongation.

Animals↗

T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants.

Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells. It was found that these monoclonal anti-CB-20 antibodies detect the new allotypic determinants (distinct from the B cell Igh-C region determinant) expressed only on the augmenting or suppressor T cells. Genetic analysis of these antigenic determinants revealed these antibodies react with the gene products located on the telomeric side chromosome of the Igh variable region gene (Igh-V) cluster. These antibodies when given in vivo caused a modification of antibody production. The antibody activity was absorbed by Con A-stimulated B10.BR (H-2b, Igh-1b), C57BL/6 (H-2b, Igh-1b), CWB (H-2b, Igh-1b), CB-20 (H-2d, Igh-1b), and BAB-14 (H-2d, Igh-1b) spleen cells, but not by Con A-stimulated C3H.SW (H-2b, Igh-1j), BALB/c (H-2d, Igh-1a), A/Sn (H-2a, Igh-1e), and C.AL-20 (H-2d, Igh-1d) spleen cells. In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice. One monoclonal antibody reacted with 4-hydroxy-3-nitrophenyl acetyl- (NP) hapten-specific augmenting T cells, and the other two batches of monoclonal antibodies reacted with NP-specific suppressor T cells of NP-mediated cutaneous responses. A mapping study with these recombinants limits the gene coding for the T cell-specific determinants to a gene within the variable region to the telomeric side of NP-VH and to the centromeric side of prealbumin. This segment is inclusive of all immunoglobulin genes, the region Owen named IgT-C, and a histocompatibility gene (H-Ig).

Animals↗

Delayed-type hypersensitivity to hen egg-white lysozyme. I. The surface phenotypes of suppressor T cells induced by intravenous injection of lysozyme-modified spleen cells, and their molecular interactions.

Suppressor T cells (Ts) induced by lysozyme-modified syngeneic lymphocytes were characterized. Hen egg-white lysozyme (HEL)-specific delayed-type hypersensitivity (DTH) was suppressed when HEL-induced Ts were transferred into naive mice. These HEL-induced Ts had surface markers of both Thy-1 antigen, and I-J gene products. The suppression of HEL-specific DTH was greatly increased, when these Ts had been enriched with HEL-coated petri dishes. Isolated anti-HEL antibodies from B10.BR or A/Sn mice were inoculated into rabbits to induce anti-cross-reactive idiotype (CRI) antibodies. The rabbit antisera were extensively absorbed with normal B10.BR or A/Sn immunoglobulins (Igs) and MOPC 104E ascites Igs to render them idiotype (Id) specific. Using these anti-CRI antibodies, we observed that these Ts possessed Id receptors on their cell surface. Results of both fluorescence techniques and cytotoxicity tests revealed that about 10% of the enriched T cells containing these Ts were Id positive. Moreover, these enriched T cells were substantially killed by anti-I-J antiserum plus complement. However, this killing was completely blocked by HEL antigen. These results suggest that both Id receptors and I-J gene products might be forming the same molecular complexes or might coexist in the vicinity of the molecule.

Animals↗

An L-form of Staphylococcus aureus adapted to a brain heart infusion medium without osmotic stabilizers.

An L-form derived from halotolerant Staphylococcus aureus Tasaki was adapted to growth in a brain heart infusion medium without any supplemental osmotically protective solutes (360 mOsm/kg). This L-form had no chemically detectable peptidoglycan residues on its surface. Electron microscopic observations confirmed morphologically the absence of the structures and also of other osmotically protective polymers within or exterior to the cytoplasmic membrane. The osmotic stability and susceptibility to bacitracin, D-cycloserine, and vancomycin of the L-form adapted to growth in 360 mOsm osmotically unprotective medium was higher than that of the L-form grown in 1,950 mOsm supplemented with 4.5% NaCl. The adapted L-form tended to be more sensitive to almost all of the antibiotics examined, other than the inhibitors for cell wall-synthesis, than the original L-form strain requiring osmotic protection for growth. Chemical analysis of the membrane of the adapted L-form indicated 16.3% total lipids and 20.6% proteins by dry weight of the membrane, and it contained larger amounts of lipid phosphorus (20.0 microgram/mg).

Anti-Bacterial Agents↗

New type of antibody-enzyme conjugate which specifically kills Candida albicans.

A new type of antibody-enzyme conjugate was made, and its possible application to Candida infection was studied. Both lactoperoxidase and xanthine oxidase were conjugated to specific antibody against Candida albicans. In vitro microbiocidal activity of the new antibody-enzyme conjugate, when incubated together with xanthine and minute amount of halides, showed a remarkable level of candidacidal ability. When the new antibody-enzyme conjugate was given to Candida-infected mice, followed by injecting xanthine and a minute amount of halides, about 50% of these heavily infected mice survived, whereas all control nontreated mice died. These data suggest that the further eleboration of this new antibody-enzyme conjugate might lead us to improve our therapeutic methods of clinical medicine.

Animals↗

Change of P-Q intervals of the electrocardiogram in the rat hearts sensitized with the killed group A streptococci.

Prolongation of P-Q interval in the anesthetized rat was observed by repeated injection of killed group A streptococci. The prolongation was clearly recognized at about the 11th week after the first injection, but afterwards P-Q interval recovered to the normal level in spite of continuous injection of killed streptococci. His bundle electrogram recorded from isolated heart revealed the prolongation of A-H interval in the treated rat. Moreover, the transmembrane action potential in the atrioventricular nodal region of treated rat was slightly deteriorated, but the action potentials in the other cardiac muscles were not changed. It was deduced from the above results that P-Q prolongation was transiently brought about by the injection of killed group A streptocci and that deterioration of muscle in the atrioventricular nodal region might take a main part in the P-Q prolongation.

Action Potentials↗

Electron microscopic study of hemadsorption on vaccinia virus infected cells.

Hemadsorption (HAD) induced in HEp-2 cells infected with vaccinia virus was observed. In ultrathin sections, binding of 36 red blood cells (RBCs) was examined in detail and 3 types of HAD were observed: (1) direct and close binding of RBCs to infected HEp-2 cells (cyto-HAD) was observed in cross sections of 27 RBCs (2) binding of RBCs through microvilli of infected cells was found in 11 RBCs, and (3) five RBCs were distorted to form tentacle-like projections by which they were bound to the HEp-2 cell surface. Scanning electron microscopy revealed that more than 30% of the RBCs were bound to microvilli of vaccinia virus-infected HEp-2 cells, and that the number of microvilli twined round each RBC was over ten, RBCs were attached to certain microvilli through swollen sucker-like tips which were not observable in non-infected HEp-2 cells. RBCs sometimes revealed a polygonal shape at regions of binding to microvilli. Virion-mediated RBC HEp-2 cell binding could not be observed.

Binding Sites, Antibody↗