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T Yokochi

Publications and source records attributed to T Yokochi.

At least 163 records · Page 9Linked to original sources
PubMed1986

Induction of human leukocyte antigen-A,B,C and -DR on cultured human oligodendrocytes and astrocytes by human gamma-interferon.

gamma-Interferon (IFN-gamma) is known to induce expression of major histocompatibility complex (MHC) class II antigens on murine astrocytes and MHC class I antigens on murine oligodendrocytes. We studied whether the human IFN-gamma could induce the expression of Human Leukocyte Antigen (HLA)-A, B, C and -DR antigens on cultured human glia from autopsied brain white matter tissue. HLA-A, B, C antigens were induced on both human astrocytes and oligodendrocytes, whereas HLA-DR antigens were induced only on some astrocytes. From these results, it is suggested that IFN-gamma affects the expression of MHC class I and class II antigens on astrocytes and oligodendrocytes derived from human brain. The relationship between the induction of MHC class I and class II antigens by IFN-gamma and the pathogenesis of multiple sclerosis is discussed.

Astrocytes↗
PubMed1986

Establishment of a murine leukemia L1210-specific T-cell clone displaying novel in vivo anti-tumor activity.

The murine leukemia L1210-specific cytotoxic T-cell clone K7 was established by repeated antigenic stimulation of spleen cells of L1210-immune CD2F1 mice in long-term culture. K7 possessed L1210-specific cytolytic activity detectable by the 51Cr-release test, but lost its cytolytic activity about 100 days after initiation of culture (designated as clone K7L). Clone K7L retained its L1210-specific tumor-growth-inhibitory activity independently of culture supplementation with IL-2. K7L possessed the cell-surface antigenic phenotype of cytotoxic T cells, Thy-1+, Lyt-1-, Lyt-2+. This clone K7L displayed surprisingly strong activity in specifically inhibiting in vivo tumor growth of L1210 by day 5 in the peritoneal cavity of CD2F1 mice when injected together with 10(5) tumor cells (more than 90% inhibition at E/T = 5), and prolonged survival times of most of the mice for more than 60 days, whereas control mice inoculated with L1210 alone died on day 9-17. This unique in vivo anti-tumor activity was not correlated to the in vitro cytolytic activity. Nevertheless, bystander inhibitory effect on the growth of third-party tumor cells (P388) was not seen in mice injected with a mixture of L1210 and P388 together with K7L, suggesting that K7L inhibited L1210 growth by direct cell-to-cell interaction. Host cells such as X-irradiation (800R)-sensitive lymphocytes and Carrageenan-sensitive macrophages were not involved in the early growth inhibition of L1210 by K7L.

Animals↗
PubMed1986

Differential expression of Epstein-Barr virus membrane antigens defined with monoclonal antibodies.

Four different mouse hybrid cell lines producing IgG2b monoclonal antibodies against Epstein-Barr virus (EBV) membrane antigens (MA) were analyzed. The antigens defined by these antibodies, MA-2, MA-4, MA-5, and MA-7, were expressed only on EBV-producing cells. The antigens were induced on P3HR-1 cells by treatment with tumor-promoting agent (TPA) plus n-butyrate, and this induction was inhibited by treatment with phosphonoacetic acid (PAA) or acyclovir. Most MA monoclonal antibodies neutralized the infectivity of EBV in vitro in the presence of complement. The monoclonal antibody MA-4 precipitated two polypeptides with mol wt of 340K and 240K, while other monoclonal antibodies MA-2, MA-5, and MA-7, did only 340K peptide. The frequency of positive cells in MA-induced cells varied for each monoclonal antibody tested. It was also found that MA-4 (anti-340K and 240K) antibody reacted on both chemically induced cells and EBV-superinfected cells, but others did only on chemically induced cells. It was suggested that MA had a different pattern of expression between chemically induced cells and EBV-superinfected cells.

Animals↗
PubMed1986

Aberrancy in immunogenicity and cell-surface expression of H-2 antigens on erythrocytes.

Immunogenicity for T cell-independent B-cell response assessed by splenic plaque-forming cell (PFC) response and cell-surface expression measured by laser flow cytometry of various class I H-2 antigens on mouse red blood cells (RBC) were compared. It was found that the order of magnitude of both immunogenicity and cell-surface expression on RBC is H-2Dd much greater than H-2Db greater than H-2Kd, H-2Kb. Furthermore, H-2d public antigens and H-2Ld antigens were neither immunogenic nor easily demonstrable on RBC. These findings contrasted with poor immunogenicity for PFC response (Nakashima et al. 1982, 1983) and proportionally strong expression of H-2 antigens on lymphoid cells. Immunogenicity and cell-surface expression of H-2Dd antigen on RBC were not shown to be controlled by the action of genes outside H-2D. It was therefore suggested that a number of H-2 antigens, including H-2Kd private, H-2Kb private, and H-2d public specificities are at least functionally defective on RBC. This is possibly due to the structural characteristics of the antigens. Since immunogenicity and cell-surface expression were in parallel, the expression of H-2 antigens on RBC must be dictated by a subset of B cells whose activity was assessed by PFC response. This finding supports the view that the H-2 molecules display a new category of activity which is different from their ability to activate T cells and depends on their expression on RBC.

Animals↗
PubMed1986

Characterization of an echovirus type 30 variant isolated from patients with aseptic meningitis.

An outbreak of echovirus type 30 infection associated with aseptic meningitis occurred among newborn babies in a hospital neonatal room at Fukui City in 1983. The isolated virus was identified as an antigenic variant of echovirus type 30 by cross-neutralization tests with antisera against the prototype Bastianni strain and the present isolate. Western blot analysis demonstrated that the antigenic determinants responsible for virus neutralization, some of which were type specific and others strain specific, were present on the capsid protein VP1. The current strain was more thermoresistant than the prototype, suggesting some alterations in virus structural proteins.

Capsid↗
PubMed1986

Microbial adjuvant and autoimmunity. IV. The induction of thyroid lesions in syngeneic X-irradiated mice by the transfer of spleen cells from mice immunized with thyroid extract and Klebsiella O3 lipopolysaccharide.

The role of humoral and cellular immune responses in the initiation and maintenance of autoimmune thyroiditis was investigated in mice immunized with syngeneic thyroid extract and Klebsiella O3 lipopolysaccharide (KO3 LPS) as an adjuvant. The transfer of spleen cells from hyperimmunized mice to 400R-irradiated syngeneic mice produced definite lesions in the thyroid glands, whereas the transfer of immune sera failed to do so. No lesions were induced in normal intact mice by the same transfer of sera and spleen cells from hyperimmunized mice. It was suggested that the induction of thyroiditis by immunization using KO3 LPS adjuvant is primarily due to cell-mediated immunity and that pretreatment of mice by X-irradiation is essential for production of the lesions. The role of X-irradiation in the induction of thyroiditis was discussed.

Adjuvants, Immunologic↗
PubMed1986

Topological and operational delineation of antigenic sites on the HN glycoprotein of Newcastle disease virus and their structural requirements.

Monoclonal antibodies to the hemagglutinin-neuraminidase glycoprotein of Newcastle disease virus have identified four antigenic sites on the glycoprotein, which are topologically and operationally discriminated from one another. To define the metabolisms and cellular compartments required for formation of the individual antigenic sites, a panel of monoclonal antibodies were examined for their reactivity with the nascent and variously processed forms of the antigen molecules in combination with the use of inhibitors of glycosylation (tunicamycin and N-methyl-1-deoxynojirimycin) and glycoprotein transport (carbonyl cyanide m-chlorophenylhydrazone and monensin). Reactivity was also examined with the antigen molecules deglycosylated by endoglycosidase F and with the antigen molecules reduced by 2-mercaptoethanol. The results taken together suggest that posttranslational organization of the glycoprotein is important for all four of the antigenic sites. At the same time, there appeared to be marked site-specific requirements with respect to glycosylation and disulfide bond formation. However, all of these metabolic requirements were found to be provided within the rough endoplasmic reticulum, and no further processing of the antigen molecules appeared to be necessary for the formation of any of the antigenic sites.

Amino Acid Sequence↗
PubMed1985

Adjuvant actions of polyclonal lymphocyte activators. V. Proliferation of macrophage colony-forming cells in the draining lymph node.

We investigated the action of various polyclonal lymphocyte activators (PLA) on the proliferation of macrophage colony-forming cells in vivo at the local site. As PLA, Klebsiella pneumoniae 03 lipopolysaccharide (K03 LPS), Escherichia coli 0111 lipopolysaccharide (E. coli LPS), dextran sulfate (DS), concanavalin A (Con A), phytohemaggulutinin (PHA), polyadenylic-polyuridylic acid (poly(A:U], polyinosinic-polycytidylic acid (poly(I:C], and pokeweed mitogen (PWM) were used. All PLA tested acted to proliferate macrophage colony-forming cells in the draining lymph node at a late stage after subcutaneous injection. The order of strength of this action of PLA was K03 LPS greater than E. coli LPS greater than Con A greater than DS greater than PHA, PWM, poly(I:C), and poly(A:U), which corresponded to the order of strength of their adjuvant action in initiating helper-T-cell response to subcutaneous injection of aggregate-free bovine gamma-globulin. The detailed relationship between the proliferation of macrophage colony-forming cells and the adjuvant action of PLA is discussed.

Adjuvants, Immunologic↗
PubMed1985

Simultaneous development of humoral and cellular tumor-specific immunity against L1210 mouse leukemia.

We have recently described that a variant of L1210 leukemia cell (L1210/LN-1) originally fused with Lesch-Nyhan fibroblast is highly immunogenic for inducing tumor-specific transplantation immunity in (BALB/cxDBA/2)F1 mice. This finding has clearly been confirmed in the present study by in-vitro cell-mediated cytotoxicity assay. Direct cytotoxic tests and competitive inhibition tests using tumor cells such as P388, LS-1 and L5178Y as target or inhibitor cells showed that the cell-mediated immunity is specific to L1210 leukemia. In the process of this study, we found that the CD2F1 mice hyperimmune to L1210 leukemia cells developed co-existing humoral anti-L1210 leukemia immunity. In an in vitro complement-dependent cytotoxicity test and absorption test, antisera from hyperimmune mice reacted specifically to L1210 leukemia cells, but not other tumor cells such as P388, L5178Y, LS-1, DB27C and BW5147 or normal cells from various tissues of DBA/2, BALB/c and AKR mice. In an in vitro cytotoxicity blocking test, the cytotoxic antisera specifically reactive to L1210 cells totally failed to inhibit lysis of L1210 cells by cytotoxic cells, suggesting that antigens recognized by cell-mediated cytotoxicity assays are not identical to serologically defined tumor-cell surface antigens.

Animals↗
PubMed1985

In vivo effects of bacterial lipopolysaccharide on proliferation of macrophage colony-forming cells in bone marrow and peripheral lymphoid tissues.

Changes in the number of macrophage colony-forming cells in various tissues of mice injected with lipopolysaccharide (LPS) from Klebsiella pneumoniae, Escherichia coli, or Salmonella enteritidis were studied. The injection of LPS increased macrophage colony-forming cells in peripheral lymphoid tissues such as the spleen, mesenteric lymph nodes, and regional lymph node, although the same treatment caused the decrease of such cells in the bone marrow. This phenomenon was consistently observed when tested by various LPSs. The injection of LPS into mice which had been exposed to X-ray irradiation and reconstituted with syngeneic normal bone marrow cells decreased colony-forming cells in the spleen. The increase of macrophage colony-forming cells in the spleen seemed, therefore, not to be due to migration from the bone marrow. The injection of LPS appeared to shorten the lag time before the initiation of mitosis of colony-forming cells in the spleen but not in the bone marrow. No participation of serum factors in this phenomenon could be detected. It was suggested that there might be an essential difference between the responsiveness to LPS of macrophage colony-forming cells in the spleen and those of the bone marrow.

Animals↗
PubMed1985

Characterization of a porcine kidney cell line resistant to influenza virus infection.

A mutant cell line of porcine kidney cells that resists the cytopathic effect of influenza virus has been obtained and characterized. These cells, designated ESK-R, were originally obtained by prolonged cultivation of cells surviving influenza B/Kanagawa/73 virus infection. No infectious virus was recovered from ESK-R cells, and no evidence for the presence of virus antigens in the cells was demonstrated by immunofluorescent staining. ESK-R cells also showed a distinct resistance to various other strains of both types A and B influenza viruses. The growth of mumps, Sendai, or Newcastle disease virus was considerably restricted, but the cell line normally supported the replication of vesicular stomatitis virus. ESK-R cells were found to lack specific receptors for influenza virus as determined by fluorescence-activated cell sorter analyses. The membrane barrier of ESK-R cells was successfully overcome by nonspecific endocytosis of calcium-coprecipitated virus particles followed by production of an appreciable amount of progeny virus.

Animals↗
PubMed1985

Strong adjuvanticity of bacterial lipopolysaccharides possessing the homopolysaccharides consisting of mannose as the O-specific polysaccharide chains.

The lipopolysaccharides (LPS) from Klebsiella 03 and 05 and Escherichia coli 08 and 09 are unique in having linear homopolysaccharides consisting of mannose as the O-specific polysaccharide chains. All four kinds of LPS were found to exhibit very strong adjuvanticity in induction of delayed-type hypersensitivity to ovalbumin in mice compared with other kinds of LPS from Klebsiella, E. coli and Salmonella. Even if the natural forms of Klebsiella 03 LPS and 01 LPS were converted to various defined uniform salt forms, their adjuvanticity did not differ significantly from that of the respective natural forms. It was concluded therefore that the difference in strength of the adjuvanticity between them is not due to the difference in their salt forms, solubility and physical state. Correspondingly, with strong adjuvanticity of Klebsiella 03 LPS and 05 LPS, their activity in enlarging the regional lymph node was also strong. Various uniform salt forms of Klebsiella 03 LPS caused stronger regional lymph node enlargement than those of Klebsiella 01 LPS. However, the activity of E. coli 08 LPS and 09 LPS in enlarging the regional lymph node was significantly weaker than that of Klebsiella 03 LPS and 05 LPS, and there were other kinds of LPS which showed a capacity to enlarge the regional lymph node similar to that of E. coli 08 LPS and 09 LPS, despite their weak adjuvanticity. Therefore, correlation did not necessarily exist between the degree of adjuvanticity of LPS and its activity in enlarging the regional lymph node.

Adjuvants, Immunologic↗
PubMed1984

Reversible resistance to the antiviral action of interferon observed in altered BHK cells resistant to HVJ (Sendai virus) infection. Brief report.

Altered baby hamster kidney (BHK-R) cells which were subcultured in the continuous presence of HVJ (hemagglutinating virus of Japan--the Sendai strain of parainfluenza 1 virus) showed a resistance to the antiviral action of both type I and II interferons. No evidence for a direct inactivation of interferon molecules during incubation of BHK-R cells was obtained. After serial subculture of BHK-R cells in growth medium free of HVJ, surface membranes with the proper sialic acid residues were restored and the cells became susceptible to the interferon action. It is suggested that binding sites for interferons might be ranked above HVJ receptors in the "receptor gradient".

Animals↗
PubMed1984

GM 58/8: a monoclonal antibody that identifies a new lineage-specific determinant expressed by myeloid progenitors (CFU-GM) and their progeny.

A cytotoxic (IgM) monoclonal antibody (McAb) raised against human erythroleukaemia cell line HEL appears specific for the myelomonocytic lineage. Indirect immunofluorescence and fluorescence-activated cell sorter analyses of peripheral blood and bone marrow cells showed that this McAb (designated GM 58/8) reacts exclusively with more than 90% of the granulocytes, monocytes and myeloid precursors. The positive (fluorescent) fraction sorted from McAb-treated bone marrow buffy coat cells showed a marked enrichment of myeloid precursors, while nonmyeloid cells were recovered in the negative fraction. GM 58/8 specifically inhibited the growth of 90-100% of the committed myelomonocytic progenitors (CFU-GM) in five complement-mediated cytotoxicity experiments. GM 58/8 had virtually no effect on the erythroid progenitor (BFU-E and CFU-E) growth. Cell sorting experiments using this McAb resulted in recovery of 84% of CFU-GM among the fluorescent fractions. Comparisons with other anti-myelomonocytic McAbs reported so far suggest that GM 58/8 has more restricted reactivity and shows more efficient CFU-GM cytotoxicity. Patterns of reactivity with normal cells and established lines indicate that the antigenic determinant identified by GM 58/8 is different from that recognized by previously described anti-myelomonocytic McAbs. McAb GM 58/8 could be used to isolate or remove pure populations of progenitors and/or more differentiated cells of the myelomonocytic lineage for in vitro studies. This study also provides evidence that the HEL cell line, derived originally from an erythroleukaemia patient, expresses an antigenic determinant shared by the normal cells of myelomonocytic lineage.

Antibodies, Monoclonal↗
PubMed1984

Anti-HEL cell monoclonal antibodies recognize determinants that are also present in hemopoietic progenitors.

The characteristics of nine monoclonal antibodies (MoAbs) produced using the uninduced cells of a human erythroleukemia line (HEL) as immunogen are described. These antibodies were grouped into four categories by their differences in recognition of normal cells and cells of hemopoietic cell lines. The four MoAbs of group A recognize determinants that are expressed in a large proportion of normal bone marrow cells and other mature cells. The two MoAbs of group B (53/5, 53/6) and the two MoAbs of group C (54/23, 54/39) recognize small proportions of bone marrow cells, whereas the single MoAb of group D (53/10) essentially recognizes only HEL cells. Competition experiments revealed two pairs of competing Abs (53/5 and 53/6; 54/23 and 54/39). In complement-dependent cytotoxicity of progenitors, 53/6 produced 90%-100% inhibition of CFU-E, BFU-E, and CFU-C growth; 54/39 30%-60% inhibition of BFU-E and CFU-C growth; 53/10 produced a variable degree of inhibition of CFU-E and BFU-E. Cell sorting using 53/6 resulted in approximately a 10-12-fold enrichment of CFU-E, BFU-E, and CFU-C among the positive cells. Cell sorting with 54/23 resulted in recovery of over 90% of BFU-E and 100% of CFU-C among the 23.5% of sorted cells showing strong or intermediate positivity. These findings suggest that HEL cells possess surface characteristics that are expressed in several classes of hemopoietic progenitors.

Animals↗
PubMed1984

Monoclonal antibodies detecting antigenic determinants with restricted expression on erythroid cells: from the erythroid committed progenitor level to the mature erythroblast.

Two new cell surface antigens specific for the erythroid lineage were defined with cytotoxic IgM monoclonal antibodies (McAb) (EP-1; EP-2) that were produced using BFU-E-derived colonies as immunogens. These two antigens are expressed on in vivo and in vitro derived adult and fetal erythroblasts, but not on erythrocytes. They are not detectable on resting lymphocytes, concanavalin-A (Con-A) activated lymphoblasts, granulocytes, and monocytes or granulocytic cells or macrophages present in peripheral blood or harvested from CFU-GM cultures. Cell line and tissue distributions distinguish McAb EP-1 and EP-2 from all previously described monoclonal antibodies. McAb EP-1 (for erythropoietic antigen-1) inhibits the formation of BFU-E and CFU-E, but not CFU-GM, colonies in complement-dependent cytotoxicity assays. By cell sorting analysis, about 90% of erythroid progenitors (CFU-E, BFU-E) were recovered in the antigen-positive fraction. Seven percent of the cells in this fraction were progenitors (versus 0.1% in the negative fraction). The expression of EP-1 antigen is greatly enhanced in K562 cells, using inducers of hemoglobin synthesis. McAb EP-2 fails to inhibit BFU-E and CFU-E colony formation in complement-dependent cytotoxicity assays. EP-2 antigen is predominantly expressed on in vitro derived immature erythroblasts, and it is weakly expressed on mature erythroblasts. The findings with McAb EP-1 provide evidence that erythroid progenitors (BFU-E and CFU-E) express determinants that fail to be expressed on other progenitor cells and hence appear to be unique to the erythroid lineage. McAb EP-1 and EP-2 are potentially useful for studies of erythroid differentiation and progenitor cell isolation.

Animals↗