PubMed Health⌕ Search

Biomedical subjects

F Sendo

Publications and source records attributed to F Sendo.

At least 109 records · Page 6Linked to original sources
PubMed1984

Activation of cytotoxic polymorphonuclear leukocytes by in vivo administration of a streptococcal preparation, OK-432.

Injection ip of a streptococcal preparation, OK-432, into WKA and DONRYU rats induced in vitro cytotoxicity of polymorphonuclear leukocytes (PMN) against tumor cells in terms of their cytostasis and cytolysis. PMN were obtained from peritoneal exudates of WKA and DONRYU rats. Cytotoxicity of activated PMN was immunologically nonspecific, although a certain target selectivity was observed in PMN cytotoxicity. The titer of cytotoxicity of PMN was dependent on the dose of injected OK-432 and on the number of PMN in the cytotoxicity assay. Activated PMN appeared very early (6 hr) after OK-432 injection, and the cytotoxic titer of PMN decreased from 24 hours and disappeared at 96 hours after injection of the reagent. In vitro culture of PMN with OK-432 also evoked cytotoxicity of PMN.

Animals↗
PubMed1983

In vitro induction of cytotoxic polymorphonuclear leukocytes by supernatant from a concanavalin A-stimulated spleen cell culture.

Rat polymorphonuclear leukocytes (PMN) pretreated with supernatant of a spleen cell culture stimulated with concanavalin A (Con A sup) inhibited 3H-thymidine uptake of various syngeneic, allogeneic, and xenogeneic tumor cells. Con A sup-treated PMN were cytostatic not only to tumor cells but also to embryonal fibroblasts and normal Con A blasts. Stimulated PMN also killed some tumor cells, as shown by 3H-uridine release assay. Cytostasis by Con A sup-treated PMN began at a very early phase of incubation, but in the cytolysis assay, incubation for more than 12 hr was required to obtain significant killing. The time required for activation of cytostatic PMN by Con A sup was short (5 min was enough) if high titers of Con A sup were used for activation. PMN-stimulating activity of Con A sup was not abrogated by treatment at 60 degrees C for 30 min or by change of pH from 1 to 11. The mechanisms of cytotoxicity by Con A sup-treated PMN are discussed.

Animals↗
PubMed1982

Nonspecific inhibition of in vivo tumor growth by allo-sensitized lymphocytes - requirement of radio-sensitive T-lymphocytes.

In previous papers we demonstrated with the Winn assay the WKA rat spleen cells sensitized to allogeneic tumor (AH-66 from Donryu strain) inhibited in vivo tumor growth of a syngeneic tumor (KMT-17) when early spleen cells (taken one week after the last immunization) were used. For the tumor inhibition by late spleen cells (2 weeks after the last immunization), further addition of inactivated homologous allogeneic cells was required. In the present study we examined with the Winn assay the nature of allo-sensitized spleen cells which nonspecifically inhibit in vivo growth of syngeneic tumors. Tumor inhibitory activity of early spleen cells was decreased by anti-rat T serum treatment. The same was true in tumor inhibition by late spleen cells stimulated with mitomycin-C treated AH-66 cells. Both of early and late spleen cells responsible for tumor inhibition are radio-sensitive, whereas KMT-17 sensitized T cells which specifically inhibited growth of homologous tumor cells belong to radio-resistant subpopulations.

Animals↗
PubMed1982

The mechanism of cholera toxin-induced suppression of natural killer cytotoxicity.

In a previous publication, it was reported that the pretreatment of mouse spleen cells with cholera toxin (CT) greatly inhibited their natural killer (NK) cytotoxicity. In the present study, it was found that ganglioside GM1 blocked the inhibitory effect of CT, and mature T cells and nylon-wool-adherent cells were not involved in the CT-mediated inhibition of NK cytotoxicity. It was also demonstrated that subunit A or B dissociated from CT lacked the capacity to inhibit NK cytotoxicity. In addition, CT-mediated inhibition was persistent and irreversible. The implications of CT-mediated inhibition of NK cytotoxicity are discussed.

Animals↗
PubMed1981

Enhancement of antitumor transplantation resistance in rats by appropriately timed administration of busulfan.

Enhancement of specific transplantation resistance to a syngeneic tumor (KMT-17) was observed in WKA rats by treatment with the antileukemia drug busulfan (BU) (15 mg/kg) 5 days before and 5 days after immunization with X-irradiated KMT-17 tumor cells. Rats immunized with X-irradiated KMT-17 cells and then treated with BU showed specific transplantation resistance only against KMT-17 tumor. Carrageenan administration after BU treatment had no effect on enhancement by BU, which indicated that macrophages were not playing a major role in the observed enhancement. With the Winn assay, it was found that spleen cells from rats immunized with X-irradiated tumor cells followed by BU inhibited the growth of admixed tumor cells more strongly than did spleen cells from rats only immunized or only BU treated and that the tumor-neutralizing activity of spleen cells from rats treated by immunization followed by BU was abrogated by treatment with anti-T-serum and complement. It was suggested that the enhanced antitumor transplantation resistance caused by BU was due to enhanced T-cell immune responses to tumor cells. Enhancement of anti-tumor transplantation resistance by BU was significantly abrogated by adoptive transfer with thymus cells and was slightly abrogated with spleen cells from rats immunized with X-irradiated KMT-17 cells 1 day before tumor challenge but receiving no other treatment. Transfer of sera from the immunized rats had no effect on enhancement by BU. These results, taken together, suggest that the mechanism of the enhancement by BU involved a selective elimination of the immunosuppressor cells from the immunized hosts.

Animals↗
PubMed1981

Augmentation of specific cell-mediated immune responses to tumor cells in tumor-bearing rats pretreated wih the antileukemia drug busulfan.

Lethal growth of a syngeneic transplanted tumor (KMT-17) was inhibited in inbred WKA rats pretreated with the antileukemia drug busulfan (BU). However, the lethal growth of KMT-17 was not inhibited by pretreatment with cyclophosphamide, adriamycin, or ftorafur. With the Winn assay, spleen cells from BU-pretreated KMT-17-bearing rats (TBR) inhibited the growth of admixed KMT-17 cells more strongly than did spleen cells from BU-untreated TBR. The augmented tumor inhibitory activity of spleen cells was KMT-17-specific, and this activity was abrogated by in vitro treatment of spleen cells with anti-T serum and guinea pig complement. Augmentation of the immune response to KMT-17-associated antigen(s) in BU-pretreated TBR was also demonstrated in lymphocyte-mediated cytotoxicity, as detected by a 51Cr release assay and by a delayed-type hypersensitivity with a radioisotope footpad assay. Tumor regression in BU-pretreated rats was demonstrated to be mediated by the augmentation of T-cell-mediated immune responses to tumor-associated antigens. The tumor inhibitory effect of BU was abrogated by adoptive transfer with thymus cells from normal rats but not with those from BU-pretreated rats 1 day before tumor inoculation. The augmentation oif the antitumor immune responses by pretreatment with BU was suggested to be due to the fact that BU selectively inhibited the suppressor cells of their precursors.

Animals↗
PubMed1981

Inhibition of mouse natural killer activity by cholera toxin.

The treatment of mouse spleen cells with cholera toxin (CT) extracted from Vibrio cholerae greatly reduced natural killer (NK) activity. The inhibition of NK activity was rapidly induced by CT treatment and persisted in the absence of CT. Even a very small amount of CT, such as 0.1 ng/ml, was effective in inhibiting NK activity. The inhibitory effect of CT on NK activity was lost upon preabsorption of CT with brain tissues, but not upon preabsorption with liver or kidney tissues.

Animals↗
PubMed1980

Non-H-2-linked genetic control of resistance to BALB/c fibrosarcoma Meth-A.

The genetic control of hybrid resistance to BALB/c fibrosarcoma Meth-A was investigated. A Meth-A tumour grew slower in (BALB/c x C57BL/6)F1 and reciprocal hybrid mice than in syngeneic BALB/c mice and was also found to grow slower in females than in males. Significant F1 resistance was demonstrated after both subcutaneous and intraperitoneal injection of tumour cells. However, (BALB/c x DBA/2)F1 mice did not show any significant resistance to Meth-A. In H-2 linkage studies of [BALB/c x (BALB/c x C57BL/6)] backcross mice, no statistically significant differences in the resistance of H-2 heterozygotes and homozygotes to Meth-A were observed. These results indicated that F1 hybrid resistance to Meth-A was controlled by non-H-2-linked resistance factor(s). No linkage was observed between resistance to Meth-A and coat colour c- and b-loci.

Animals↗
PubMed1978

Spontaneous regression of syngeneic transplanted tumors in rats pretreated with the antileukemia drug busulfan.

Lethal growth of a syngeneic transplanted tumor (KMT-17) was inhibited in WKA rats pretreated with the antileukemia drug busulfan. The effect of busulfan was short-lasting, and administration of the drug after tumor challenge had little effect on the lethal growth of the tumor. After spontaneous regression of the tumor in rats pretreated with busulfan, specific transplantation resistance to identical tumor was acquired. Busulfan did not exhibit its effect in rats irradiated before tumor challenge. As shown by the Winn test, spleen cells from rats immunized with inactivated tumor cells after busulfan treatment inhibited growth of admixed tumor cells more strongly than did spleen cells from rats immunized without busulfan treatment. Enhancement of immune response to tumor cells rather than tumoricidal activity by busulfan was suggested.

Animals↗
PubMed1978

Regression of established tumors in rats by injection of diethylaminoethyl-dextran and Friend murine leukemia virus.

Subcutaneously established tumors in WKA rats were treated with polycation DEAE-dextran (DEAE-D) and Friend murine leukemia virus (F-MuLV). This idea was based on "xenogenization of tumors," which is defined as the immunologic regression of transplanted tumors in syngeneic rats after artificial infection of tumors with murine leukemia viruses. Regressions of subcutaneously established tumors were induced in 13 of 40 (33%) rats by injection of DEAE-D and F-MuLV. Intratumor injections of DEAE-D and F-MuLV increased the regression of tumors in 7 of 12 (58%) rats as compared to that of tumors in 6 of 28 (21%) rats treated with DEAE-D and F-MuLV by other injection routes. Electron-microscopic and immunofluorescence examinations revealed that tumor cells were infected with F-MuLV and acquired F-MuLV-related surface antigen on the cell surfaces. Therefore, the regression in rats of subcutaneously established tumors by the injection of DEAE-D and F-MuLV may have been due to an immunologic mechanism that may have been the same as the xenogenization of transplanted tumors previously infected with murine leukemia viruses.

Animals↗
PubMed1977

Anti-tumour immunity by normal allogeneic blood transfusion in rat.

Growth of transplantable KMT-17 tumour in syngeneic WKA/MK rats was inhibited by i.v. preimmunization with whole blood from normal rats of allogeneic strains. The inhibitory effect was also observed in rats immunized with allogeneic white blood cells alone. The strength of the inhibitory effect mainly depended on the the strain of donor rat used; blood from Donryu and Kyoto strain rats produced the strongest inhibition, blood from Tokyo and Fischer strain rats produced moderate inhibition to the syngeneic tumour growth. Blood from ACI/N strain rats did not produce the inhibition. The mechanism of blood transfusion in inhibiting tumour growth is not yet clear. However, it seems that GVH reaction does not play an important role in the mechanism of the inhibition effect, because the effect was obtained by immunization with mitomycin C-treated allogeneic white blood cells and also by the immunization effect may be due to nonspecific active immunization. Significance of blood transfusion with special reference to clinical immunogtherapy of cancer is discussed.

Animals↗
PubMed1977

Effect of x-irradiation of recipients on in vivo neutralization of syngeneic tumors by spleen cells nonspecificially immunized with allogeneic tumors.

Spleen cells from WKA rats immunized with allogeneic Donryu tumor (AH66), when examined by the Winn test, inhibited lethal growth of admixed antigenically unrelated syngeneic tumor (KMT-17) only when a mixture of spleen cells and tumor cells was injected into pre-irradiated recipients. On the other hand, spleen cells specificially sensitized to KMT-17 inhibited growth of admixed KMT-17 cells either in irradiated or non-irradiated rats.

Animals↗
PubMed1976

Inhibition of syngeneic tumor growth in rats immunized with allogeneic skin grafts.

The growth of a transplantable tumor (KMT-17) in syngeneic Wistar King Aptekman/Mk (WKA) rats was inhibited by preimmunization with allogeneic normal cells from Donryu strain rats. The phenomenon is referred to as allogeneic cell immunity. A slight inhibition was observed in rats immunized with normal liver, spleen, kidney, embryonal cells, whole blood and white blood cells from allogeneic Donryu rats. A strong inhibition was observed in animals which had rejected allogeneic skin grafts, particularly from the Donryu and Kyoto rats. The inhibition was comparatively weak after immunization with skin grafts from the Long Evans, ACI, Buffalo, Ficsher, Sprague Dawley or Tokyo allogeneic rat strains. This immunizing effect was dependent on the viability of the grafts and was easily abrogated by low-dose irradiation. The mechanism of allogeneic cell immunity is considered to be a non-specific stimulation of the immunity against antigenic tumors in the syngeneic host

Animals↗