Showing papers by "Ken-ichi Isobe published in 1989"

Induction of Antitumor Immunity in Mice by Allo-Major Histocompatibility Complex Class I Gene Transfectant With Strong Antigen Expression

Abstract: An allo-major histocompatibility complex class I gene (H-2Kb) was transfected to murine mastocytoma P1.HTR (P815 subline) cells, after which several transfectant clones were obtained. Two clones, which expressed a low level of H-2Kb antigen, grew well and killed the syngeneic DBA/2 mice when they were inoculated ip. These mice lived longer than the mice given injections of the parental P1.HTR tumor. However, one clone, which expressed a high level of H-2Kb antigen, was rejected completely by the syngeneic DBA/2 mice and induced a generation of H-2Kb-specific cytotoxic T cells. Interestingly, the mice that had rejected the clone with high H-2Kb expression received strong anti-tumor immunity for rejection of the parental P1.HTR tumor challenged at the high dose.

Rat mesangial cells actively produce phosphatidylinositol-anchored Thy-1.

Abstract: We provide evidence that the mesangial cells of rat kidney glomeruli express Thy-1 as a phosphatidylinositol-anchored protein. Both the mesangial area of kidney, examined in tissue sections, and mesangial cells maintained in culture for more than 3 months, showed prominent immunofluorescence staining with an anti-Thy-1 monoclonal antibody (OX7); this staining was almost completely abolished by pretreating kidney sections or mesangial cells with the phosphatidylinositol-specific enzyme, phospholipase C. By Northern blotting, mesangial cells were shown to express mRNA of an appropriate size, hybridizing to a mouse Thy-1.1-specific probe.

Carbohydrates mediate tissue type-specific membrane activity for Thy-1 alloantibody response.

Abstract: Thymocyte membrane fragments (TMF) but not brain cell membrane fragments (BMF) show a unique activity for inducing Thy-1 alloantibody response. Treatment of TMF with alpha-mannosidase or endoglycosidase-H greatly diminished this activity but not the serological Thy-1 antigenicity. This suggested that the TMF activity is supported by high mannose type N-linked oligosaccharides on the TMF. On the other hand, treatment with neuraminidase made otherwise silent BMF definitely active for the antibody response and this activity was abolished by further treatment with endoglycosidase-D. This demonstrated that BMF have a latent activity which is mediated by complex type N-linked oligosaccharides normally masked with sialic acids. It was concluded that two types of N-linked oligosaccharides as well as sialic acids mediate at least in part the tissue type-specific membrane activity for Thy-1 alloantibody response.

Donor Igh-linked genetic control of allotype-specific antibody response

Abstract: Immunogenicity of allogeneic immunoglobulins in mice were studied, measuring the allotype-specific antibody activity by agglutination of allogeneic antibody-coated red blood cells. It was found that the serum from C.B-20 mice (Ighb, BALB/c-congenic) was uniquely immunogenic in BALB/c mice for allotype antibody response. Whereas the C57BL/6 (Ighb) serum was immunogenic only when heat aggregated and/or combined with adjuvant, the ultracentrifugation-deaggregated C.B-20 serum was definitely immunogenic when administered in a moderate dose (100 μl/mouse). Even more surprising was the fast that very low doses (0.01–0.1 μl) of soluble C.B-20 serum, but not C57BL/6 serum, down regulated the allotype-specific response effectively. Genetic analysis on congenic mice suggested that the immunogenicity is controlled by donorIgh orIgh-V(Id-C.B) inasmuch as the serum from BALB/c-congenic C.B-20 (Igh-VbCb), but not BALB/c-congenic BAB/14 (Igh-VaCb), mice was active in BALB/c mice in soluble form. Further studies showed that the Id-C.B was dominantly expressed on the immunoglobulins of (BALB/c×C.B-20)F1 and (C56BL/6×C.B-20)F1 strains, and was originally derived from the C57BL/Ka strain. The major determinant for the antibody production was encoded inIgh-C, but not inIgh-V. It is suggested thatId-C.B controls the allotype-specific antibody response in an unusual manner, possibly acting as a unique determinant activating helper T cells.