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1.
A 3 M KCl crude extract of the syngeneic benzpyrene-induced fibrosarcoma termed BP 238 specifically inhibits migration out of glass capillary tubes of immune spleen cells from tumor amputee and small tumor-bearing rats, as does supernatant medium from tumor cells grown in culture. Serum from rats bearing small (< 2 cm3) tumors does not inhibit migration of immune spleen cells, while serum from rats with larger tumors (>4 cm3) nonspecifically inhibits migration of both immune and nonimmune spleen cells, thoracic duct lymphocytes, and thymocytes. This nonspecific inhibition increases with increasing tumor size, does not correlate with the presence of bacterial infection, and is presumably due to a circulating factor produced in vivo during tumor growth. Production of macrophage inhibitory-like factor (MILF) by neoplasms in vivo may offer a mechanism for tumors to escape immunosurveillance by systemic immobilization of cytotoxic lymphocytes. From Sephadex and ultrafiltration fractionation experiments, the molecular weight of MILF in serum is polydisperse (30,000–100,000 daltons), and is heat and chymotrypsin resistant, in contrast with the properties reported for LIF (leukocyte inhibitory factor) and MIF (macrophage migration inhibitory factor) produced in vitro.  相似文献   

2.
Summary The immunogenicity of KMT-17 fibrosarcoma cells which had been xenogenized by infection with FV was compared to that of KMT-17 cells which had been admixed with BCG. We report here that 105 and 106 KMT-17 cells also grew progressively to kill rats, but when 105 KMT-17 cells were administered with BCG the tumor cells did not grow in the majority of rats. The strength of immunogenicity (ETD50), as measured by the number of immunizing cells required for a suppression of growth of 107 KMT-17 cells in 50% of the rats, was 2.1×103 for FV-KMT-17 and 36.3×103 for BCG+KMT-17. The tumor cell dose (LTD50) which was required to kill 50% of the rats immunized with 105 FV-KMT-17 was more than 10,000 times higher than that found in normal rats, whereas the number of tumor cells required to kill 50% of the rats immunized with the same number of BCG+KMT-17 was only 3,680 times higher than the amount found in normal rats. Thus the immunogenicity of FV-KMT-17 is much stronger than that of BCG+KMT-17.The difference in immunogenicity between the two vaccines was also observed in the tumor-neutralizing activities of spleen cells obtained from rats which had been immunized with both vaccines, as measured by a Winn assay. Moreover, the antitumor activity of spleen cells from rats immunized with FV-KMT-17 was concentrated in the carrageenan-resistant and plastic nonadherent cells, while that of spleen cells from rats immunized with BCG+KMT-17 was observed in carrageenan-sensitive and plastic adherent cells as well as in nonadherent cells. The involvement of different effector cells indicates that different mechanisms operate in the antitumor resistance in rats immunized with either FV-KMT-17 or BCG+KMT-17. Abbreviations used: FV, Friend leukemia virus; FV-KMT-17, Friend leukemia virus infected KMT-17 cells; EDT50, a 50% effective tumor dose; LTD50, a 50% lethal tumor dose  相似文献   

3.
The authors tested the ability of scattered tumor cells to re-form a tumor in vivo. Disseminated tumor cells are morphologically visible stained with May-Grünwald Giemsa in the lung, liver, kidney, and spleen of Yoshida ascites tumor bearing rats. Free tumor cells can easily be fine needle aspirated from those organs and injected in syngeneic Wistar rats. All the host rats show ascites tumor take after intraperitoneal transplantation of each aspirated sample. This biological model might be useful to study in vivo a wide range of properties of neoplastic and non-neoplastic host cells.  相似文献   

4.
Inbred C57BL/6 (B6) mice which had received an inoculation of allogeneic spleen cells showed remarkable antitumor activity against syngeneic tumor challenge with B16 melanoma cells 3 days after the allogeneic cell inoculation. This antitumor activity was not specific to the inoculated alloantigen, since the challenging B16 cells are syngeneic to B6 mice and since it was induced by BALB/c spleen cells as well as C3H/He spleen cells. The antitumor activity was sensitive to an in vivo treatment with anti-asialo GM1 (AGM1) antiserum or anti-Thy.1 monoclonal antibody (mAb) just before the tumor challenge and was resistant to an in vivo treatment with anti-CD8 (Ly. 2) mAb. These results suggest that AGM1+Thy.1+CD8– activated natural killer (NK) cells were generated by alloantigen inoculation and took an important part in the antitumor effect of the alloantigen inoculation.  相似文献   

5.
EMMPRIN has a role in invasion and metastasis through the induction of MMPs and the consequent modulation of cell-substrate and cell–cell adhesion processes. The present study evaluates the expression of EMMPRIN protein and MMP-2/9 activity in tumor and parenchymal cells in a spontaneous metastasis model in rats. Moreover, we explore the regulation of EMMPRIN and MMP-9 by tumor-epithelial cell interactions in vitro. By zymography, we observed an increased proMMP-9 expression in both metastasized liver and spleen samples from tumor bearing rats. Immunohistochemical studies showed EMMPRIN-positive tumor cells in tumor biopsies as well as in spleen and liver samples from tumor bearing rats. Interestingly, a significant increase in EMMPRIN expression in hepatic cells was also detected. The regulation of EMMPRIN expression in tumor and liver cells in response to tumor–host interaction was investigated in vitro through a tumor cell line culture on extracellular matrix (ECM) molecules or in co-culture with normal rat liver cells (BRL3A cells). No significant changes in EMMPRIN expression were detected in tumor cells cultured on ECM molecules. On the other hand, EMMPRIN protein and MMP-9 mRNA expression were induced in BRL3A cells. The increase in EMMPRIN expression in BRL3A cells was inhibited by an anti-EMMPRIN antibody. These results reinforce the main role of EMMPRIN mediating tumor–host interactions that may evolve new opportunities for therapeutic interventions.  相似文献   

6.
Summary The role of antigen-reactive cell opsonization (ARCO) in a syngeneic tumor system and its effect on tumor progression was investigated. Thus, anti-tumor reactive T cells were prepared in vivo by immunization of normal SJL/J mice with mitomycin C-inactivated tumor cells of the syngeneic transplantable reticulum cell sarcoma (RCS) line LA-6. Dividing cells were subsequently labeled by injecting iodo-2-deoxyuridine (125IUdR) into the same animals 3 days later. Antigen-reactive cells (*ARC) present in the radiolabeled, nylon wool-fractionated spleen cell population taken from these mice on day 4 and injected IV into syngeneic SJL/J mice bearing LA-6 tumors were diverted to the liver and away from the spleen. The effect was maximal by 8 days following inoculation of tumor cells, and was specific inasmuch as 125IUdR-labeled cells prepared by immunization with allogeneic spleen or tumor cells which were not opsonized in day-8 LA-6 tumor-bearing mice. Opsonization of *ARC in day-8 LA-6 tumor-bearing mice was completely abrogated by either prior injection of heat-aggregated immunoglobulin into the mice or preincubation of the *ARC in solubilized tumor antigen before injection into tumor-bearing mice, demonstrating the involvement of Fc receptors in the host and antigen-specific receptors on the *ARC, respectively, in the opsonizing process. When anti-LA-6 reactive T cells were incubated in serum from LA-6 tumor-bearing mice and then injected IV into normal syngeneic SJL/J mice, a similar liver diversion was observed. Serum from cyclophosphamide-pretreated mice injected with LA-6 or serum from mice given mitomycin C-inactivated LA-6 cells did not cause opsonization of tumor-reactive T cells, while a mixture of these two sera did have some *ARC opsonizing activity. Further experiments with SJL/J mice bearing spontaneous RCS tumor indicate that tumor-reactive T cells are also opsonized in these mice. The above studies and others suggested that ARCO may play an important role in vivo in the survival of tumors. Abbreviations used in this paper are: ARC, antigen-reactive cells; ARC, radiolabeled antigen-reactive cells; ARCO, antigen-reactive cell opsonization; LA-6 tumor line derived in our laboratory; L.I., localization index; PEG, polyethylene glycol; RCS, reticulum cell sarcoma; STA, soluble tumor antigen; TBS, tumor-bearer serum  相似文献   

7.
The delayed type hypersensitivity response to human serum albumin (HSA) of rats infected intraperitoneally with 107 viable C. neoformans cells, and 7 days after, immunized with human serum albumin was significantly diminished (p<0.05) when compared with the response observed in rats immunized with human serum albumin and non infected. The spleen mononuclear cells from suppressed rats transferred to normal syngeneic recipients of the same sex suppress the afferent phase of the response (p<0.02) suggesting that cells present in the spleen might be one of the responsible mechanisms for the suppression to nonrelated antigens in infected animals.  相似文献   

8.
Parenteral immunization of mice with a given strain of type A influenza virus generates two subpopulations of cytotoxic T cells in the in vivo primary response. One subpopulation is specific for the immunizing virus; the other subpopulation cross-reacts with target cells infected with type A influenza virus of a different subtype. Both subpopulations are specific for target cells infected with type A influenza virus and optimally lyse only infected targets which are syngeneic at the H-2 gene locus. In vitro stimulation of previously primed spleen cells with cells infected with homologous virus generates both subpopulations in the secondary cytotoxic response. However, in vitro stimulation of primed cells with cells infected with heterologous type A virus of a different subtype specifically selects for the cross-reactive T-cell population. These results are discussed in terms of current models for T-cell recognition of virus-infected cells and possible mechanisms for cross-reaction between type A influenza viruses of different subtypes at the level of cytotoxic T cells.  相似文献   

9.
Summary The effects of a variety of adjuvant protocols on immunoglobulin levels in normal and tumor bearing CBA mice have been investigated together with their ability to elicit immunoglobulin which bind to tumor cells in vitro and inhibit the growth of a transplanted syngeneic MC-induced fibrosarcoma.A marked increase in serum levels of certain immunoglobulins (especially IgG 2a , IgG 2b and IgM) and immunoglobulin interacting with tumor cells in vitro was noted in normal and tumor bearing mice following the administration of C. parvum (strain No. CN6134 and 10387), P. freudenreichii (strain No. 10470) and B. pertussis while a modest increase in some of these accompanied BCG injection. The Freund's complete and incomplete adjuvant protocols adopted had little effect on any of these parameters. The C. parvum protocols alone inhibited tumor growth.The immunoglobulins evoked by C. parvum strain No. 6134 which bound to tumor cells in vitro were extremely heterogeneous, activity being detected in all Ig classes and subclasses. This organism also evoked immunoglobulins which interacted with syngeneic embryonic fibroblasts, and adult syngeneic kidney and spleen cells.Tumor cells which had been preincubated in sera rich in immunoglobulins binding to tumor cells in vitro (i.e. from C. parvum-treated mice) did not exhibit reduced growth following i.v. or s.c. transplantation to syngeneic recipients.  相似文献   

10.
The migration of splenic T and B lymphocytes into syngeneic tumors undergoing immunologic rejection was investigates. Spleen cells were obtained from normal BALC/c mice or BALB/c mice bearing tumors induced by murine sarcoma virus (MSV). Either whole spleen cells or immunoabsorbent purified T and B cells were radiolabeled with sodium chromate-51 and injected i.v. into normal or MSV inducted-tumor bearing syngeneic recipients. Twenty-four hours later the recipient mice were sacrificed and radioactivity was assessed for tumor, contralateral normal muscle, the lymph nodes draining the tumor and contralateral draining lymph nodes, peripheral lymph nodes, spleen, and liver. Both T and B lymphocytes from either normal or MSV tumor-bearing animals show greatly increased migration into the tumor when compared with normal muscle. Migration of T cells from both normal and MSV tumor bearers was 30 times that of migration to normal muscle. B cells from tumor-bearing mice, on the other hand, localized in the tumor itself only 50% as frequently as did B cells from normal animals. In addition, T cells from MSV tumor bearers were found in the highest proportion in the lymph node draining the tumor site. We conclude that T and B lymphocytes from either normal or tumor-bearing mice migrate to a syngeneic tumor undergoing immunologic rejection. In contrast, the migration of both T and B cells from tumor-bearing animals was decreased to the peripheral lymph nodes at the time of maximum tumor growth.  相似文献   

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