Eiji Terada

Establishment of a new murine-phenotypic angiosarcoma cell line (ISOS-1)

A cell line, designated ISOS-1, was established from a tumor formed by transplantation of a human angiosarcoma into mice with severe combined immunodeficiency (SCID). The cells showed endothelial properties, based on the uptake of Dil-Ac-LDL and binding of UEA-I/GSA-I lectins, but were negative for CD11b and Pan Cytokeratin. However, the cells lost differentiated characteristics such as expression of von Willebrand factor, contact inhibition growth and tube formation activity. These findings indicate that ISOS-1 is a poorly-differentiated endothelial cell line. At the 81st passage, all of the cells were positive for H-2Dd in various intensity, but not HLA-ABC. The metaphase chromosomes consistently showed a characteristic mouse, but not human, telocentric form. Furthermore, this cell line produced fatal tumor growth in SCID mice and also in BALB/c mice. These results suggest that ISOS-1 is a murine-phenotypic angiosarcoma cell line.

Cyclosporin A-Induced Suppression of Ongoing IgE Antibody Formation in the Mouse

Persistent anti-ovalbumin (OA) IgE antibody formation in the mouse was suppressed by oral administration of cyclosporin A (Cy A). Spontaneous anti-OA IgE antibody formation in vitro was also suppresse

Interstitial pneumonitis in autoimmune MRLlpr mice and its treatment with cyclosporin A

Age-associated changes of anti-double-stranded (ds) DNA antibodies, anti-single-stranded (ss) DNA antibodies, and serum immune complex concentrations were studied in MRL/lpr mice. All anti-ds DNA antibodies, anti-ss DNA antibodies, and immune complexes began to be detected in the sera of MRL/lpr mice aged 8 to 13 weeks and increased remarkably after 17 weeks of age. Almost no pathological findings were observed histologically in the lungs of MRL/lpr mice aged 8 weeks but interstitial pneumonitis became evident at 14 weeks of age. Peribronchial and perivascular lymphocyte infiltrations were seen in the lungs of 14-week-old MRL/lpr mice and became more severe at 21 weeks of age. Oral administration of cyclosporin A to 15-week-old MRL/lpr mice markedly prolonged their life span. The lungs of 44-week-old MRL/lpr mice given cyclosporin A showed few pathological findings except for minimal perivascular lymphocyte infiltration.

A solid-phase enzyme immunoassay for anti-acetylcholine receptor antibody in myasthenia gravis patients

A solid-phase enzyme immunoassay for the measurement of anti-acetylcholine receptor antibodies in the sera of patients with myasthenia gravis is reported. Sufficient amounts of acetylcholine receptor for the sensitive detection of anti-acetylcholine receptor antibody were directly fixed to Costar serocluster 96-well EIA plates coated with poly-L-lysine hydrobromide. The solid-phase enzyme immunoassay detected anti-acetylcholine receptor antibodies in 91% of the myasthenia gravis patients including 4 out of 4 ocular type myasthenia patients, anti-acetylcholine receptor antibodies of which were not detectable by the immunoprecipitation assay. Correlation between antibody titers measured by enzyme immunoassay and the immunoprecipitation assay was significant.

Detection of mouse hepatitis virus antibody by protein A-ELISA in 6 prevalent inbred strains or outbred stocks of mice

Protein A was applied as a reagent for the secondary reaction in ELISA (protein A-ELISA). Mouse hepatitis virus antibody in 6 prevalent mouse strains or stocks reared in a MHV-contaminated room was effectively detected by protein A-ELISA, whereas significant strain differences in the antibody detection rate were demonstrated using the complement fixation test. C57BL/6 mice were particularly reactive in the protein A-ELISA test.

IgE-isotype-specific suppressor cells in the mouse: characterization using tetraparental chimera mice of high (DBA/2) and low (SJL) IgE responder embryos.

Tetraparental chimera mice were developed by aggregation of IgE high responder (DBA/2) and IgE low responder (SJL) embryos. Anti-dinitrophenyl (DNP) IgE antibody response in such mice (SJL----DBA/2) upon challenge with DNP-keyhole-limpet hemocyanin (KLH) in alum was clearly suppressed, while anti-DNP IgG antibody response was not. High-titer anti-DNP IgE and IgG antibody response developed in F1 hybrid mice of SJL and DBA/2 (SDF1) mice. The experimental results suggest that high IgE antibody production is the dominant trait, and the IgE-specific suppressor gene in SJL mice is autosomal recessive. IgE-specific suppressor T cells in SJL mice actively suppressed IgE antibody formation by DBA/2 immuno-competent cells across the histocompatibility barrier. Hapten-specific B cells and carrier-specific T cells were prepared in SJL----DBA/2 and SDF1 mice by immunization with DNP-KLH or ovalbumin (OA) in alum and transferred to irradiated SDF1 mice followed by challenge with DNP-OA. Hapten-specific B cells and carrier-specific helper T cells clearly developed in SDF1 mice. Recipient mice transferred with DNP-KLH-primed SDF1 spleen cells and OA-primed SDF1 spleen cells showed high-titer anti-DNP IgE and IgG antibody responses. OA-primed SJL----DBA/2 spleen cells cotransferred with DNP-KLH-primed SDF1 spleen cells and OA-primed SDF1 spleen cells completely abolished secondary anti-DNP IgE antibody response. The data suggest that carrier-specific helper T cells for IgE and IgG antibody responses are distinct. The regulatory role of IgE-isotype-specific suppressor cells were considered to be the interference of cooperative cellular interaction between IgE B cells and carrier-specific, IgE-specific helper T cells.