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T Hamaoka

Publications and source records attributed to T Hamaoka.

At least 271 records · Page 15Linked to original sources
PubMed1985

Dystrophic axons in the nucleus gracilis of the normal rat containing cholecystokinin-like immunoreactivity. Light- and electron-microscopic observations.

Cholecystokinin immunoreactive (CCKI) axons in the nucleus gracilis of the normal rat were studied by light and electron microscopy using the peroxidase-antiperoxidase (PAP) immunocytochemical method. Immunoreactivity was found in both normal and dystrophic axons at various ages. Slightly enlarged CCKI varicosities were first observed in 2-month-old rats, gradually increased in number (max. at 21 months) and in diameter (up to 20 micron at 21 months), and then decreased (at 27 and 36 months). Dilatated CCKI fibers continuous with dystrophic varicosities also tended to increase proportionally in diameter. The dystrophic CCKI axonal profiles, first identified at the light-microscopic level and then observed under electron microscopy, had consistently characteristic features. In addition, numerous dystrophic nonreactive axonal profiles had morphological features differing from those of dystrophic reactive ones at advanced ages. These findings suggest that CCK may be partly involved in the formation of dystrophic axons in the nucleus gracilis.

Aging↗
PubMed1985

[Automated autoradiographic grain counting of DNA repair in cultured human fibroblasts after ultraviolet irradiation].

Measurement of autoradiographic grains produced by the decay of incorporated radioisotopes is often used for a quantitative assay of the rate of DNA replication and DNA repair in cells or tissues. However, visual grain counting by microscopic observation is time-consuming and tedious process. Recently, Kraemer et al. reported that automated measurement of grains in cultured human cells may be facilitated by using appropriate grain counting instruments. Under their experimental conditions using Kodak NTB-3 emulsion, instrument-determined grain number per nucleus was proportional to visual counts up to 30 grains, and then leveled off at much larger visual counts. The saturation phenomenon was due to counting-loss by the instrument caused by overlapping of neighboring grains. To prevent the counting-loss, we have used in the present study Japanese Sakura NR-M2 emulsion which is less sensitive to radiation exposure than Kodak NTB-3, thereby yielding smaller size of grains per radioactive decay. Samples were prepared from cultured skin fibroblasts derived from normal individuals and xeroderma pigmentosum (XP) patients defective in DNA repair. These cells were irradiated with 254 nm UV incubated for 3 h with culture medium containing 3H-thymidine, and autoradiograms were made by dipping in Sakura NR-M2 emulsion. The number of grains as well as grain surface area per nucleus was measured by using ARTEK CYTO TALLY MODEL 900 counting instrument, and compared with visual counts. The results showed that, under our optimum condition, the instrument-determined number of grains was directly proportional to visual counts, at least up to 150 grains per nucleus, with a correlation coefficient of 0.971.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoradiography↗
PubMed1985

Studies on the induction of tolerance to alloantigens. I. The abrogation of potentials for delayed-type-hypersensitivity response to alloantigens by portal venous inoculation with allogeneic cells.

The present study investigates the effect of portal venous (p.v.) administration of allogeneic cells on the capacity of delayed-type-hypersensitivity (DTH) reactivity to alloantigens. BALB/c mice were inoculated with C3H/He spleen cells via intravenous (i.v.) or p.v. route. Intravenous injection of C3H/He spleen cells into BALB/c mice resulted in appreciable DTH responses to C3H/He alloantigens. In contrast, p.v. inoculation of the same number of C3H/He cells not only failed to induce any significant anti-C3H/He DTH responses but also abolished the capability of the animals to develop DTH responses as induced by subcutaneous (s.c.) immunization with C3H/He spleen cells. Such suppression was alloantigen-specific, since p.v. inoculation of C3H/He spleen cells resulted in selective inhibition of anti-C3H/He DTH potential without suppressing DTH responses to C57BL/6 alloantigens. This tolerance was rapidly inducible and long-lasting. When spleen cells from tolerant mice were transferred i.v. into 600 R X-irradiated syngeneic recipient mice alone or together with normal BALB/c spleen cells, these tolerant spleen cells themselves failed to induce DTH responses but did not exhibit any suppressive effect on the generation of DTH responses induced by normal spleen cells co-transferred. These results indicate that tolerance was not necessarily associated with the induction of suppressor cell activity but rather was associated with the elimination or functional impairment of clones specific for alloantigens. The results are discussed in the context of a) the role of the liver in immune responses, b) cellular mechanisms underlying the tolerance induction, and c) potential application of this approach to the future transplantation immunology.

Animals↗
PubMed1985

Immunoregulation in the rat: cellular and molecular requirements for B cell responses to types 1, 2, and T-dependent antigens.

The requirements for primary in vitro plaque-forming cell (PFC) development in cultures of purified rat splenic B cells have been examined. Rat B cells were directly responsive to the type 1 antigen trinitrophenyl-Brucella abortus (TNP-BA), but both T cells and adherent accessory cells were required for B cell responses to the type 2 antigen TNP-Ficoll and the T cell-dependent (TD) antigen sheep erythrocytes (SRBC). However, the cellfree supernatants from concanavalin A-induced spleen cells of rat or mouse origin replaced the requirement for T cells and macrophages, and resulted in PFC development in response to TNP-Ficoll and SRBC and augmented PFC numbers in response to TNP-BA. Culture supernatants from induced murine T cell and macrophage cell lines were used to partially deduce the molecular requirements for the support of PFC development by rat B cells to these three antigens. Supernatants from the EL-4 (EL-4 sup) and B151 K12 (B15 sup) T cell lines augmented TNP-BA responses, suggesting that B cell growth factor II (BCGF-II) mediated this effect. An admixture of purified interleukin 2 (IL 2) and B15 sup supported PFC development to SRBC; indicating that IL 2, BCGF-II, and the T cell-replacing factor in B15 sup (B15-TRF) were sufficient to support this response. In addition, the IL 2 plus B15 sup-supported anti-SRBC PFC response was increased by the addition of an interleukin 1-containing fraction from the supernatant of the macrophage line P388D1. PFC development in response to TNP-Ficoll had the most stringent requirements and only occurred in the presence of EL-4 sup and B15 sup (IL 2, BCGF-I, BCGF-II, EL-TRF, B15-TRF). These data indicate that different cellular and molecular requirements exist for PFC development in response to types 1, 2, and TD antigens by rat B cells.

Animals↗
PubMed1985

The mechanism of tolerance induction of tumor-specific delayed-type hypersensitivity responses by intravenous inoculation of tumor cells.

C3H/HeN mice were inoculated intravenously (iv) with 10(6) 10000-R X-irradiated syngeneic MCH-1-A1 fibrosarcoma cells 3 times at 4-day intervals (pretreatment). Spleen cells from these pretreated or normal mice were sensitized in vitro to MCH-1-A1 tumor cells and effector cells generated after 5 days of culture were assayed for delayed-type hypersensitivity (DTH) responses by an adoptive transfer into footpads of syngeneic recipient mice together with MCH-1-A1 cells. Normal spleen cells stimulated with MCH-1-A1 tumor cells generated appreciable anti-MCH-1-A1 DTH responses, whereas spleen cells from the above pretreated mice failed to induce anti-MCH-1-A1 DTH responses. These pretreated spleen cells did not inhibit the generation of DTH responses when co-cultured with normal spleen cells as responding cells. Since vaccinia virus-reactive helper T cells are capable of enhancing DTH responses against antigens co-expressed on vaccinia-infected cells, their ability to augment anti-MCH-1-A1 DTH responses from the pretreated spleen cells upon stimulation with vaccinia-infected MCH-1-A1 cells was investigated. The results demonstrate that under conditions in which enhanced anti-MCH-1-A1 DTH responses were obtained by supplementing vaccinia helper T cells, these vaccinia-helpers were not able to generate any significant DTH responses from the pretreated spleen cells. These results indicate that iv inoculation of tumor cells suppresses the generation of tumor-specific DTH responses not by inducing suppressor cell activity, but rather by inhibiting DTH effector clones themselves.

Animals↗
PubMed1985

Small and large B cells respond differently to T cell-derived B cell growth and differentiation factors.

A major problem in B cell biology is the determination of the roles played by helper T (TH) cells vs cytokines in the activation, replication, and differentiation of B lymphocytes. There is general agreement that activated B cells in cycle can replicate and terminally differentiate when provided with appropriate T cell-derived lymphokines. There is considerable controversy, however, as to whether cytokines can induce resting G0 B cells to secrete IgM. Some reports claim that TH cells are required before cytokines can act. In contrast, other reports claim that some T cell-derived supernatants (SN) have the capacity to activate resting B cells to become immunoglobulin-secreting cells. In the present study, we have examined one such SN (S26.5) as well as the EL-4 and PK 7.1 SN for their capacity to activate resting G0 B cells and a population of less dense B cells containing activated cells. These two populations, separated by Percoll density centrifugation, were characterized for size, stage in the cell cycle, and cell surface phenotype. It was shown that the most dense population contained predominantly G0 B cells, whereas the less dense population contained a subset of cells in cycle. Our studies show that neither T cell SN nor, indeed, any combination of cytokines and anti-immunoglobulins caused a major increase in the number of cells secreting IgM in the population enriched in G0 cells. In contrast, the T cell SN caused marked increases in the generation of IgM secreting cells in the population that contained a large proportion of activated cells. Limiting dilution analysis confirmed that the number of responding cells in the dense cell population was substantially lower than the number of responding cells in the less dense population. The small number of precursors in the dense B cell population may be attributed to contamination of that population with cells that have undergone activation steps in vivo. The present results, therefore, add further evidence to an existing large body of evidence that TH cells are essential for the terminal differentiation of G0 resting B cells in response to thymus-dependent antigens.

Animals↗
PubMed1985

T-T cell interaction in the induction of delayed-type hypersensitivity (DTH) responses: vaccinia virus-reactive helper T cell activity involved in enhanced in vivo induction of DTH responses and its application to augmentation of tumor-specific DTH responses.

The role of antigen-specific helper T cells in augmenting the in vivo development of delayed-type hypersensitivity (DTH) responses was investigated. C3H/HeN mice were inoculated i.p. with vaccinia virus to generate virus-reactive helper T cell activity. These vaccinia virus-primed or unprimed mice were subsequently immunized subcutaneously (s.c.) with either trinitrophenyl (TNP)-modified syngeneic spleen cells (TNP-self), vaccinia virus-infected spleen cells (virus-self), or cells modified with TNP subsequent to virus infection (virus-self-TNP). Seven days later, these mice were tested for anti-TNP DTH responses either by challenging them directly with TNP-self into footpads or by utilizing a local adoptive transfer system. The results demonstrated that vaccinia virus-primed mice failed to generate significant anti-TNP DTH responses when s.c. immunization was provided by either virus-self or TNP-self alone. In contrast, vaccinia virus-primed mice, but not unprimed mice, could generate augmented anti-TNP DTH responses when immunized with virus-self-TNP. Anti-vaccinia virus-reactive helper activity was successfully transferred into 600 R x-irradiated unprimed syngeneic mice by injecting i.v. spleen cells from virus-primed mice. These helper T cells were found to be antigen specific and were mediated by Thy-1+, Lyt-1+2- cells. DTH effector cells enhanced by helper T cells were also antigen specific and were of the Thy-1+, Lyt-1+2- phenotype. Furthermore, vaccinia virus-reactive helper T cell activity could be applied to augment the induction of tumor-specific DTH responses by immunization with vaccinia virus-infected syngeneic X5563 tumor cells. T-T cell interaction between Lyt-1+ helper T cells and Lyt-1+ DTH effector T cells is discussed in the light of the augmenting mechanism of in vivo anti-tumor-specific immune responses.

Animals↗
PubMed1985

Genetic control of hapten-reactive helper T-cell responses and its implications for the generation of augmented antitumor cytotoxic responses.

The genetic control of hapten-reactive helper T-cell activity involved in cytotoxic T-lymphocyte (CTL) responses and its implications for augmenting tumor-specific immunity were studied. C57BL/6N mice were immunized to trinitrophenyl (TNP) or N-iodoacetyl-N'-(5-sulfonic l-naphthyl)ethylenediamine (AED) hapten by inoculation of hapten-modified syngeneic spleen cells. Spleen cells from these hapten-immunized mice were tested for hapten-reactive helper T-cell activity for generation of CTL. TNP-primed spleen cells resulted in only marginal help for the generation of anti-TNP-modified syngeneic spleen cell (TNP-self) CTL response when cocultured with normal C57BL/6N spleen cells (responding cells) in the presence of TNP-self. In contrast, AED-primed spleen cells exhibited appreciable help for AED-induced CTL responses. Furthermore, AED-helper, but not TNP-helper, T-cell activity was demonstrated to augment the generation of antitumor (RBL-5 leukemia) CTL responses from normal syngeneic spleen cells when stimulated with the corresponding hapten-self plus RBL-5 tumor cells. These results indicate that the successful augmentation of syngeneic tumor immunity through T-T-cell interaction with the use of hapten-reactive helper T-cells can depend on selection of the appropriate haptenic reagent in an individual expressing a given major histocompatibility haplotype.

Animals↗
PubMed1985

Purification and physicochemical characterization of murine T cell replacing factor (TRF).

Murine T cell replacing factor (TRF) was purified from a cellfree supernatant of a T cell hybridoma (B151K12) that constitutively produces TRF. Two assay systems for TRF activity were employed: 1) induction of anti-DNP IgG PFC responses in cultures of splenic B cells from DNP-KLH-primed BALB/c mice, and 2) induction of IgM PFC in chronic B cell leukemic cells (BCL1). The purification scheme consisted of ammonium sulfate precipitation, DEAE-cellulose chromatography, Blue-Sepharose chromatography, hydroxylapatite chromatography, gel permeation with fast protein liquid chromatography (FPLC), and disc polyacrylamide gel electrophoresis. Overall, TRF was purified approximately 34,000-fold with a maximum 3.8% recovery of activity, and the specific activity of the purified TRF was approximately 9.6 X 10(4) U/mg. The TRF that is active in these systems is distinct from the other lymphokines such as IL 1, IL 2, BCGFI (now known as BSFp1), and gamma-interferon. The TRF is extremely hydrophobic, with an apparent m.w. of 50,000 to 60,000 on gel permeation chromatography and 18,000 on SDS-PAGE under reducing conditions. Highly purified B151-TRF abrogated the activity by treatment with trypsin but not with RNase. Moreover, it bound to lima bean agglutinin-Sepharose specific for N-acetylgalactosamine residues, indicating that B151-TRF is a glycosylated glycoprotein containing N-acetylgalactosamine residues. The role of N-acetylgalactosamine residues on TRF activity was additionally substantiated by the fact that the addition of appropriate amounts of N-acetylgalactosamine in the assay systems for TRF preferentially induced a profound suppression for TRF-mediated PFC responses.

Adjuvants, Immunologic↗
PubMed1985

Cell-mediated T lymphocyte responses against syngeneic cells modified with amino-reactive hapten (AED-NH2): H-2Dk serves as an element for cell-mediated lympholysis to amino-reactive hapten (AED-NH2)-modified self.

Spleen cells from C3H/He mice immunized to the newly synthesized amino-reactive hapten, 5-sulfo-1-naphthoxy acetic acid N-hydroxysuccinimide (AED-NH2), were stimulated in vitro with AED-NH2 modified syngeneic cells. After 5 days of culture, effector cells were assayed for their cytotoxic activity against AED-NH2-modified target blast cells. In contrast to other amino-reactive haptens reported so far, a strong cytotoxic activity against AED-NH2-modified syngeneic cells was found in H-2b mice as well as in H-2k mice. Furthermore, Dk-restricted anti-AED-NH2 CTL recognition was observed in H-2k mice as shown by cold target inhibition. Previous studies have demonstrated the predominant influence of K over D region self determinants, and of the chemical reactivity of the haptenic reagent in Ir gene control of CTL response to hapten-self. The present report illustrates the importance of the hapten itself in genetic regulation of these CTL responses.

Animals↗
PubMed1985

The mechanism of tumor growth inhibition by tumor-specific Lyt-1+2-T cells. I. Antitumor effect of Lyt-1+2-T cells depends on the existence of adherent cells.

In the present study we establish an assay system of tumor growth inhibition with the use of a diffusion chamber and investigate the mechanism by which tumor-specific Lyt-1+2-T cells exhibit their inhibiting effect on tumor cell growth. When a diffusion chamber containing X5563 plasmacytoma cells together with normal syngeneic C3H/HeN spleen cells was implanted in the peritoneal cavity of C3H/HeN mice, these tumor cells continued to proliferate at least 7 to 9 days. In contrast, spleen cells from C3H/HeN mice that had acquired X5563-specific immunity by intradermal (i.d.) inoculation of viable tumor cells, followed by surgical resection of the tumor, exhibited an appreciable inhibitory effect on the growth of X5563 tumor cells admixed in the chamber. This antitumor effect was mediated by Lyt-1+2-T cells and was tumor-specific, because the growth of X5563 or another syngeneic MH134 hepatoma cells was inhibited by spleen cells from C3H/HeN mice immunized to the respective tumor cell types. Most important, these tumor-specific Lyt-1+2-T cells lost their antitumor activity by depleting an adherent cell population contained in spleen cells, indicating that adherent cells are required for the Lyt-1+2-T cell-mediated antitumor effect. This was substantiated by the fact that immune spleen cells depleted of adherent cells could regain their tumor-inhibiting effect when normal spleen cells were added back as an adherent cell source, or more directly by adding back a splenic or peritoneal resident adherent cell population. These results indicate that tumor-specific Lyt-1+2-T cells mediate the tumor growth inhibition and that their antitumor effect depends on the coexistence of an adherent cell population.

Animals↗
PubMed1985

Studies on macrophage-activating factor (MAF) in antitumor immune responses. I. Tumor-specific Lyt-1+2- T cells are required for producing MAF able to generate cytolytic as well as cytostatic macrophages.

In the present study we investigated some of the cellular mechanisms for the generation of macrophage-activating factor(s) (MAF) in immune responses to tumor antigens. C3H/HeN mice were immunized to syngeneic MH134 hepatoma or MCH-1-A1 fibrosarcoma by intradermal inoculation of viable tumor cells, followed by the surgical resection of the tumor. Spleen and lymph node cells from these tumor-immune mice were stimulated in vitro with the corresponding tumor cells, and supernatant from such a culture was tested for an ability to activate macrophages to exert their cytostatic and cytolytic activities as detected on tumor cells unrelated to immunizing tumors. Peritoneal adherent cells as a macrophage source, which were preincubated with supernatant from co-culture of tumor-unimmunized normal spleen and lymph node cells plus tumor cells, failed to exhibit any significant antitumor effect on unrelated X5563 tumor cells, whereas the addition of supernatant from cultures containing immune lymphocytes to adherent cells resulted in appreciably potent cytostatic and cytolytic effects on X5563 tumor cells, indicating the generation of MAF in culture supernatant. The activation of tumor-immune spleen and lymph node cells for MAF generation was tumor-specific, because anti-MH134- and anti-MCH-1-A1-immune lymphocytes produced MAF by the stimulation with the respective but not with the other alternative tumor cells. Such MAF production was abolished by treatment of tumor-immune spleen and lymph node cells with anti-Thy-1.2 or anti-Lyt-1.1 but not with anti-Lyt-2.1 antibody plus complement before culturing. These results indicate that the tumor-specific Lyt-1+2- T cell subset has a crucial role in generating MAF by which an adherent cell population as a source of macrophages acquires the potential for inducing a cytolytic as well as a cytostatic effect on tumor cells.

Animals↗
PubMed1985

Role of N-acetyl-D-galactosamine residue on B151K12-derived T cell-replacing factor (B151-TRF) molecule in B cell-receptor binding and -stimulating activity.

The role of sugar moiety on T cell-replacing factor molecule derived from a monoclonal T cell hybridoma B151K12 (B151-TRF) was analyzed with respect to the interaction with receptor on B cells. The induction of B cell differentiation into Ig-secreting cells by B151-TRF was specifically inhibited by addition of N-acetyl-D-galactosamine (GalNAc) to culture. Such inhibition appeared to be attributed to the interference of GalNAc in the interaction of TRF with its receptor, because absorption of TRF activity with B cells was notably inhibited by the presence of GalNAc. To substantiate this point further, we established binding assay of B151-TRF molecule to the receptor on B cells by using 125I-labeled TRF fraction enriched by reversed-phase high-performance liquid chromatography and gel filtration. The results revealed that the binding of 125I-TRF molecule to the B cells was almost completely blocked by GalNAc. Moreover, the existence of GalNAc residue(s) on B151-TRF molecule was evidenced by the facts that 1) the TRF activity was eluted from lectin gels with specificity for GalNAc as revealed by the functional assay, and 2) the 125I-TRF molecule specifically bound to such lectin gels. Thus, the GalNAc residue(s) on B151-TRF molecule plays an important role in binding of TRF molecule to the receptor and in the stimulation of B cells. The molecular properties of B cell-stimulatory B151-TRF and its mode of interaction with corresponding receptor on B cells were discussed in the context of B151-TRF as a glycosylated lymphokine molecule and B151-TRF receptor as a carbohydrate-binding protein (animal lectin).

Absorption↗
PubMed1985

Enhanced induction of tumor-specific Lyt-1+2- T cell-mediated protective immunity by in vivo administration of interleukin 1.

The present study deals with the effect of in vivo administration of interleukin 1 (IL 1) on the induction of tumor-specific immunity. Culture fluid supernatant (CFS) containing IL 1 was obtained by stimulating J774.1 cells with lipopolysaccharide. C3H/HeN mice were inoculated intradermally with viable syngeneic X5563 tumor cells, followed by five consecutive subcutaneous or intraperitoneal inoculations of IL 1-containing CFS. Lymph node and spleen cells from IL 1-CFS-treated or -untreated C3H/HeN mice 8 days after the tumor inoculation were tested for 1) cytotoxic T lymphocyte (CTL) responses as measured by subsequent in vitro sensitization with X5563 cells, 2) delayed-type hypersensitivity (DTH) responses as measured by utilizing a local adoptive transfer, and 3) tumor-neutralizing activity in a Winn assay. Lymph node cells or spleen cells from IL 1-CFS-treated X5563 tumor-bearing mice not only exhibited enhanced CTL and DTH responses, but also produced complete tumor neutralization, in contrast with cells from IL 1-CFS-untreated X5563 tumor-bearing mice. In vivo protective immunity augmented by IL 1-CFS was tumor-specific and Lyt-1+2- T cell-mediated. The molecules responsible for enhanced induction of tumor-specific immunity co-migrated with IL 1 activity on gel filtration. These results indicate that IL 1 has the potential to augment tumor-specific Lyt-1+2- T cell-mediated in vivo protective immunity in tumor-bearing hosts.

Animals↗
PubMed1985

Murine tumor cell lysis by antibody-dependent macrophage-mediated cytotoxicity using syngeneic monoclonal antibodies.

Four monoclonal antibodies to MH134 murine syngeneic hepatoma cells, 3H1, 7C2, 11G2, and 12A2, were produced by hybridomas constructed by fusing P3-X63-Ag8-U1 murine myeloma cells with spleen cells of a C3H/HeN mouse immunized with the syngeneic tumor cells. Immunodiffusion analysis with rabbit anti-mouse immunoglobulin antisera showed that 3H1, 7C2, 11G2, and 12A2 are IgG2a, IgM, IgG1, and IgG2a, respectively. Enzyme-linked immunosorbent assay using cells of five syngeneic tumor lines, MH134, MM102, MM46, MM48, and X5563, and lymph node cells of C3H/HeN and C57BL/6 mice showed that 3H1 specifically bound to MH134 tumor cells, whereas 7C2, 11G2, and 12A2 reacted not only with MH134 but also with MM102 and MM46 tumor cells. None of these monoclonal antibodies bound either to cells of MM48 or X5563 tumor lines or to normal lymph node cells. These results strongly suggest that MH134 tumor cells display at least two kinds of tumor-associated antigens on their cell surfaces: one is expressed uniquely by MH134 tumor cells, which are recognized by 3H1; the other is commonly shared by MH134, MM102, and MM46 tumor cells, which are determined by the other three antibodies. 3H1, 11G2, and 12A2 but not 7C2 were found to be able to induce antibody-dependent cellular cytotoxicity (ADCC) against MH134 tumor cells. Target specificity of ADCC induced by these monoclonal antibodies was identical with that seen in enzyme-linked immunosorbent assay. 3H1, 7C2, and 12A2 but not 11G2 exhibited complement-dependent cytotoxicity, showing the same specificity in target cell lysis as that seen in enzyme-linked immunosorbent assay or ADCC. Pretreatment of MH134 tumor cells with 7C2 inhibited ADCC of both 11G2 and 12A2. Pretreatment of the tumor cells with 11G2 inhibited complement-dependent cytotoxicity of both 7C2 and 12A2. Neither ADCC nor complement-dependent cytotoxicity of 3H1 was inhibited by the pretreatment of the cells with 7C2 or 11G2. These results strongly suggest that tumor-associated antigens recognized by 3H1 are located apart from that recognized by 7C2, 11G2, and 12A2 and that the binding sites of the latter three antibodies are closely associated with, or identical with, each other in the tumor-associated antigen. The ability of 12A2 to induce ADCC against MH134 tumor cells was significantly stronger than that of 3H1 or 11G2.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Prevention of tumor metastasis after surgical removal of primary tumor by using in vitro activated macrophages.

In vitro activation of peritoneal macrophages by Propionibacterium acnes and its immunotherapeutic potential for inhibiting metastasis was investigated. C3H/HeN mouse adherent peritoneal exudate cells as a source of macrophages were treated in vitro with P. acnes. These P. acnes-activated macrophages were tested for tumoricidal activity in vitro and antimetastatic activity in vivo. In vitro cytotoxicity tests revealed that they had potent cytotoxicity. Surgical resection of X5563 tumors in syngeneic C3H/HeN mice 10 days after the tumor implantation failed to rescue the hosts from tumor metastasis despite successful removal of the primary tumor. When the activated macrophages were transferred intravenously into C3H/HeN mice following the surgical operation, an appreciable number of mice survived without exhibiting any sign of metastasis. Thus, these results demonstrate that macrophages can be activated in vitro by utilizing appropriate stimulating reagents, and that these activated macrophages have a potent antimetastatic effect.

Animals↗
PubMed1985

Low plasma cholecystokinin response after ingestion of a test meal in patients with chronic pancreatitis.

Postprandial responses of plasma cholecystokinin (CCK) in patients with severe chronic pancreatitis (n = 7) were studied. Plasma CCK level rose from 11.2 +/- 1.8 pg/ml at the basal level to a maximum of 23.3 +/- 3.0 pg/ml at 10 min after the ingestion of a liquid meal in healthy subjects (n = 6). However, such significant plasma CCK response to the meal was not observed in patients with chronic pancreatitis in whom CCK levels rose from a basal level of 9.7 +/- 0.91 pg/ml to a peak of 13.8 +/- 1.6 pg/ml at 60 min. It is suggested that the low response of CCK after the meal might reflect impaired function of the enteropancreatic axis to intraluminal stimuli in patients with severe chronic pancreatitis.

Adult↗