Biomedical subjects
Publications and source records attributed to T Aoki.
The tissue-culture cell line HT-29, derived from a primary colon adenocarcinoma and previously shown to secrete carcinoembryonic antigen (CEA), was examined by immunoelectron microscopy for the location of CEA in relation to the cells. CEA was closely adjacent to the plasma membrane, a location indistinguishable from that of alloantigens and other tumor-associated antigens.
When Abelson murine leukemia virus (MuLV-A) was inoculated into pristane-primed BALB/c mice, either plasmacytomas (PCT), lymphosarcomas, or their mixed form was induced with a shorter latent period than that for PCT induction in mice treated with pristane alone. All 3 neoplasms were designated Abelson's tumors. The morphology of the induced malignant cells and the presence of known surface antigens were analyzed by electron microscopy. The cell surface antigens (CSA) examined were PC1, X.1, Gross (GCSA), and Moloney (MCSA); viral envelope antigens (VEA) were xVEA, x1-VEA, sub-gsVEA, and MVEA. MuLV-A-pristane-induced PCT cells produced markedly fewer intracisternal type-A particles than did mineral oil-induced PCT cells. Most, if not all, mineral oil-induced PCT cells carried PC1 antigen and produced many extracellular type-C viruses carrying xVEA and x1-VEA, whereas Abelson's tumor cells had both a lower incidence and a smaller amount of PC1 and X.1 antigens and xVEA+ virus and lacked x1-VEA+ virus. In addition, most Abelson's tumors and their type-C viruses did not carry MCSA and MVEA ro GCSA and sub-gsVEA. All the macrophages in the PC1+ Abelson's tumors and many macrophages in PC1-Abelson's tumors contained various amounts of PC1 on their cell surfaces. For these reasons, Abelson's tumors were clearly distinct from pristane- or mineral oil-induced BALB/c PCT and from M-MuLV- ro G-MuLV-induced tumors.
Drug-resistant gram-negative bacilli conferred with R factors were isolated with high frequencies from the intestinal tracts of ayu (Plecoglossus altivelis) cultured in ponds, in which chemotherapeutics had often been used, and with relatively low frequencies from ayu which received no administration of chemotherapeutics. Drug-resistant bacteria were also isolated at low frequencies from the intestinal tracts of wild ayu in rivers, as well as from the water of ayu-culturing ponds and some of them carried R factors. The drug-resistant bacteria carrying R factors were Aeromonas liquefaciens, Citrobacter, Enterobacter cloacae, Escherichia coli, Hafnia and unidentified strains. All the R factors were classified as the Fi-(F) type, except the two R factors detected in an E. coli strain and in an unidentified strain.
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When viral envelope antigens (VEAs) and virus-associated cell surface antigens (CSAs) are used as markers of type C viruses, more heterogeneity of virus populations can be demonstrated than by using host range alone. In the present study, four CSAs (PC1, X.1, GCSA, and MEV-SA1) and three VEAs (xVEA, x1-VEA, and sub-gsVEA) were used as markers of virus populations present in various sublines of the BALB/c embryonic fibroblast BALB/3T3 clone A31 line. Of four spontaneously transformed sublines, two released N-tropic endogenous type C viruses spontaneously after long-term culture and each had distinct antigenic patterns. Treatment with 5-bromodoxyuridine (BrdU) resulted in the detection of X-tropic viruses in all four sublines. The expression of these X-tropic viruses was associated with two different antigenic patterns. When the clonal rabbit corneal SIRC cell line was infected with the X-tropic viruses obtained after BrdU treatment, the cells acquired detectable amounts of only one of the antigenic markers.
Arabinogalactan purified from heat-killed tubercle bacilli failed to elicit a delayed type of skin reaction and had no ability to induce in vitro lymphocyte blast formation in sensitized guinea pigs. It was, however, inhibitory to migration of bronchoalveolar washing cells by the indirect test, but not by the direct test, and capable of eliciting an immediate type of skin reaction and anaphylaxis when injected into sensitized guinea pigs. Tuberculin active peptide (TAP) was active in all of in vitro and in vivo cell-mediated immune responses, but not in immediate responses.
A preparation (OK-432) of a low virulence strain, Su, of Streptococcus hemolyticus (Group A) has been found to possess 2 different effects on tumor cells: a) A direct pharmacological effect like other antitumor drugs, and b) an indirect effect through the enhancement of the host immune response. In order to examine the second effect, 2 different antigen systems were used, Gross (G) cell surface antigens (GCSAs) and the cell surface differentiation antigen PCl. At certain ages, untreated C57BL/6 and BALB/c mice occasionally produce natural antibodies to GCSAs and PCl, respectively. When the mice were injected intraperitoneally (i.p.) with OK-432 at 2 months of age, they produced natural antibodies to GCSAs or to PCl antigen, unlike untreated mice of the same strains at the same ages (negative controls), which produced no antibodies. The specificity of the antibodies was carefully examined by cytotoxicity tests. In addition, the activity of the natural antibodies was not neutralized with OK-432 itself. We have proven that OK-432 enhances the production of natural antibodies to specific cell-surface antigens.
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D1-murine leukemia virus (MuLV), an N-tropic type-C virus isolated from a spontaneous reticulum cell neoplasm, type B (RCN-B) of an SJL/J mouse was propagated in NIH Swiss mouse embryo cell cultures. When injected into BALB/c mice 1 day after neonatal thymectomy, 30% of the inoculated mice developed RCN-B in 5 months, whereas none of the uninoculated controls did. From the spleen and lymph node extracts of all RCN-B-bearing mice tested, B-tropic type-C viruses (designated E1-MuLV) were isolated in high titers (10-5 minus 10-6 XC plaque-forming units/ml). Only low titers (10-1 minus 10-2 XC plaque-forming units/ml) of N- or B-tropic viruses were isolated from those thymectomized mice, inoculated but nontumorous, whereas only N-tropic viruses were detected in the uninoculated thymectomized mice. No virus was isolated from the nonthymectomized, untreated controls. Antigenically, the viral envelope antigen (VEA) of E1-MuLV was distinct from those of DU-MuLV, xVEA, or Gross-VEA, but some cross reaction with AKR-MuLV-VEA was observed. The relationship of D1-MuLV to E1-MuVL with respect to oncogenesis and viral genome activation was discussed.
Adult AKR and C58 mice injected intramuscularly with murine sarcoma virus, Moloney isolate (M-MSV), developed high incidence of nonregressing local tumors. Histologically, these tumors revealed the typical pleomorphism of M-MSV sarcomas; in some cases, however, neoplastic tissue showed a nodular or diffuse growth of monomorphic myoblastlike cells, reminiscent of clonal aggregates. No depression of immune reactivity was found in M-MSV-injected mice as evaluated by direct hemolytic plaque-forming cells against SRBC and by virus-neutralizing antibody production. The MSV recovered from the induced tumors proved to be, by neutralization assay, a Gross (G)-MSV pseudotype. Moreover, tumor cell suspensions absorbed out cytotoxic antibody directed against G-cell surface antigens. Therefore, the conclusion was drawn that MSV with envelope characteristics of endogenous G leukemia virus had formed in vivo through a phenotypic mixing phenomenon. The failure of tumors to regress has been interpreted as mainly due to the partial unresponsiveness of host immune reactivity towards G-MuLV specified antigens. Since MSV-tumors arose in AKR mice after a very long latent period, the possibility was considered that this relative resistance might depend on immunologic mechanisms. In fact, M-MSV-injected AKR mice immunodepressed by goat antimouse lymphocyte serum or rendered partially tolerant by neonatal M-MuLV inoculation developed sarcomas with higher incidence and with a shorter latency. Furthermore, the MSV recovered from these early tumors proved to be the original Moloney pseudotype.
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