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Results for “tumor immunity”

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At least 19 recordsLinked to original sources
PubMed1971

Tumor immunity: tumor suppression in vivo initiated by soluble products of specifically stimulated lymphocytes.

Supernatant fluids of specifically stimulated lymphocyte cultures were purified. Fractions containing migration inhibition factor when injected intra-dermally into strain-2 guinea pigs produced a reaction similar in appearance to delayed cutaneous hypersensitivity. There was an accumulation of mononuclear cells at the injection sites and the growth of syngeneic tumor grafts at the sites was suppressed.

Animals↗
PubMed2003

Role of IL-13 in regulation of anti-tumor immunity and tumor growth.

Major mediators of anti-tumor immunity are CD4(+) T(h)1 cells and CD8(+) cytotoxic T lymphocytes (CTLs). In tumor-bearing animals, the T(h)1- and CTL-mediated anti-tumor immunity is down-regulated in multiple ways. Better understanding of negative regulatory pathways of tumor immunity is crucial for the development of anti-tumor vaccines and immunotherapies. Since immune deviation toward T(h)2 suppresses T(h)1 development, it has been thought that induction affecting a T(h)2 immune response is one of the mechanisms that down-regulate effective tumor immune responses. Recent studies using T(h)2-deficient signal transducer and activator (Stat6) KO mice demonstrated that this hypothesis was the case. IL-13 is one of the T(h)2 cytokines that has very similar features to IL-4 through sharing some receptor components and Stat6 signal transduction. It has been thought that IL-13 is not as critical for immune deviation as IL-4 since it cannot directly act on T cells. However, recent studies of IL-13 reveal that this cytokine plays a critical role in many aspects of immune regulation. Studies from our lab and others indicate that IL-13 is central to a novel immunoregulatory pathway in which NKT cells suppress tumor immunosurveillance. Here we will describe biological properties and functions of IL-13, its role in the negative regulation of anti-tumor immunity, and effects of IL-13 on tumor cells themselves.

Animals↗
PubMed1979

Influence of different routes of anti-tumor immunization: alternative induction of tumor immunity and tumor enhancement.

Chickens and quails were immunized in parallel either i.v. or intramuscularly (i.m.) with lectin column-purified antigens from chick embryo cells that were transformed in vitro by avain sarcoma virus (ASV). After five to six injections, immunity of the animals was tested by challenge with ASV into the wing webs. Whereas tumor growth was inhibited after i.v. immunization with respect to incidence rate and time of tumor appearance, tumor growth was enhanced after i.m. injection. Animals that were injected with normal cell antigens served as controls. Spleen cells from only those animals that were immunized i.v. exerted a cytotoxic effect in vitro against ASV-transformed cells, whereas spleen cells from i.m. injected animals, in contrast, suppressed such cytotoxicity. The search for serum blocking or arming factors suggested that sera from i.m. injected animals block cellular cytotoxicity whereas sera from i.v. immunized animals render normal spleen cells cytotoxic (arming effect). The use of viruses from different subgroups and of antigens from gp85-lacking ASV-transformed cells indicates that immune effects were obtained against tumor cell surface antigens that differ from the antigen that is involved in virus neutralization (s-gp85).

Alpharetrovirus↗
PubMed1993

Costimulation of T cells for tumor immunity.

Tumor specific antigens can be demonstrated on many neoplasms by immunization and challenge experiments; however, these antigens do not normally elicit a sufficiently strong immune response to prevent tumor growth in immunocompetent hosts. Recent studies have demonstrated that efficient activation of T cells requires costimulation of the CD28 receptor via the B7 molecule on antigen-presenting cells. Inadequate costimulation of tumor-reactive T cells may contribute to the fact that antigenic tumors are not normally rejected by the immune system, and weak anti-tumor immune responses may be amplified by upregulation of CD28 triggering.

Animals↗
PubMed2001

Enhancement of anti-tumor immunity by tumor cells transfected with the secondary lymphoid tissue chemokine EBI-1-ligand chemokine and stromal cell-derived factor-1alpha chemokine genes.

Several new lymphocyte-specific chemokines, which attract naive and memory T cells, B cells, dendritic cells and natural killer cells, have been isolated. We have found evidence of the anti-tumor effects of 3 major lymphocyte-specific chemokines, secondary lymphoid tissue chemokine (SLC), EBI-1-ligand chemokine (ELC) and stromal cell-derived factor (SDF)-1alpha, in murine models (Meth A fibrosarcoma and HM-1 ovarian tumor). In both naive and immunized mice, tumors expressing SLC, ELC or SDF-1alpha showed delayed progression compared with control tumors. In mice immunized with tumor cells expressing 1 of these 3 chemokine genes, challenge with parental tumor cells resulted in slightly slower progression than in control mice, while in mice immunized with tumor cells transfected to co-express IL-2 or granulocyte-macrophage colony-stimulating factor (GM-CSF) as well as these chemokines, all tumors regressed. Furthermore, spleen cells from mice immunized with these "double-transfected" tumor cells exhibited higher proliferative responses and greater cytotoxic activity against parental tumor cells. These anti-tumor effects were associated with profound alterations in the leukocyte populations within the tumors and regional lymph nodes, and this was due to activation of type I T cell-dependent responses that produced high levels of IFN-gamma. These findings show that SLC, ELC and SDF-1alpha enhance anti-tumor immunity both systemically and locally and that these chemokines may be clinically useful, especially when combined with IL-2 and GM-CSF.

Animals↗
PubMed1998

Heteroclitic immunization induces tumor immunity.

In tumor transplantation models in mice, cytotoxic T lymphocytes (CTLs) are typically the primary effector cells. CTLs recognize major histocompatibility complex (MHC) class I-associated peptides expressed by tumors, leading to tumor rejection. Peptides presented by cancer cells can originate from viral proteins, normal self-proteins regulated during differentiation, or altered proteins derived from genetic alterations. However, many tumor peptides recognized by CTLs are poor immunogens, unable to induce activation and differentiation of effector CTLs. We used MHC binding motifs and the knowledge of class I:peptide:TCR structure to design heteroclitic CTL vaccines that exploit the expression of poorly immunogenic tumor peptides. The in vivo potency of this approach was demonstrated using viral and self-(differentiation) antigens as models. First, a synthetic variant of a viral antigen was expressed as a tumor antigen, and heteroclitic immunization with peptides and DNA was used to protect against tumor challenge and elicit regression of 3-d tumors. Second, a peptide from a relevant self-antigen of the tyrosinase family expressed by melanoma cells was used to design a heteroclitic peptide vaccine that successfully induced tumor protection. These results establish the in vivo applicability of heteroclitic immunization against tumors, including immunity to poorly immunogenic self-proteins.

Amino Acid Sequence↗
PubMed1991

A discrete model for immune surveillance, tumor immunity and cancer.

In this paper we propose a model of tumor immunity in terms of discrete automata where each automation describes the concentration of one particular type of cell involved in immune response. In contrast to the earlier models of normal immune response, there is more than one type of cell surface antigen in this model. As a consequence, the tumor can evade destruction through humoral response by changing its identity. However, the tumor can be killed by the killer cells through cell-mediated response unless protected by a high concentration of the suppressor T cells.

Computer Simulation↗
PubMed1988

[Influence of radiation doses in local radiotherapy on anti-tumor immunity and tumor metastasis].

The relationship between radiation doses and the subsequent metastasis formation after local radiotherapy against a rat transplantable fibrosarcoma was studied. KMT-17 fibrosarcoma cells were transplanted into the hind leg of syngeneic WKA rats and the leg were irradiated with various doses of 60Co gamma-rays 5 days after the tumor transplantation. 97% of the local primary tumors regressed in the rats received more than 45Gy (high dose-group), whereas only 41% of the tumors regressed in the rats received less than 40Gy (low dose-group). On the other hand, the percentage of the subsequent metastasis in the high dose-group was significantly higher than that of the low dose-group. By Winn's assay, stronger tumor-neutralizing activities were observed in the spleen cells of rats received 30Gy than those of non-irradiated rats or rats received 60Gy. The above results suggest that the low dose irradiation to the local tumor stimulates the anti-tumor immunity which results in suppression of the tumor metastasis.

Animals↗
PubMed2004

Silencing of SOCS1 enhances antigen presentation by dendritic cells and antigen-specific anti-tumor immunity.

Tumor vaccines represent a promising therapeutic approach, but thus far have achieved only limited success in the clinic. The major challenge is to find a means of overcoming inhibitory immune regulatory mechanisms and eliciting effective T-cell responses to antigens preferentially expressed by tumor cells. Here we show that the stimulatory capacity of dendritic cells (DCs) and the magnitude of adaptive immunity are critically regulated by the suppressor of cytokine signaling (SOCS) 1 in DCs. Silencing SOCS1 in antigen-presenting DCs strongly enhances antigen-specific anti-tumor immunity. Our findings indicate that SOCS1 represents an inhibitory mechanism for qualitatively and quantitatively controlling antigen presentation by DCs and the magnitude of adaptive immunity. This study has implications for understanding the regulation of antigen presentation and for developing more effective tumor vaccines by silencing the critical brake in antigen presentation.

Animals↗
PubMed2003

CD25+ regulatory T cells and tumor immunity.

Tumor cells express a range of antigens including self-antigens (those whose expression is shared by normal host tissue) and non-self antigens (such as those that arise as a result of mutations in normal cellular genes or in the case of some tumors, viral antigens). Immune responses to both types of antigen have been identified in human patients with cancer and in murine tumor models. In both cases, these responses are typically weak and generally fail to result in tumor rejection. Accumulating evidence indicates that a population of T cells, namely CD25(+) regulatory cells, is at least partly responsible for the poor immunogenicity of tumor cells. This evidence is discussed in the context of a murine model of melanoma.

Animals↗
PubMed1984

Treatment of disseminated leukemia with cyclophosphamide and immune cells: tumor immunity reflects long-term persistence of tumor-specific donor T cells.

B6 mice bearing disseminated syngeneic FBL leukemia can be cured by treatment on day 5 with 180 mg/kg cyclophosphamide and 2 x 10(7) adoptively transferred syngeneic immune spleen cells. Complete tumor eradication in this model requires more than 30 days and is dependent upon the transfer of specifically immune T cells. To evaluate the relative contributions of host and donor T cells to tumor elimination and the maintenance of tumor immunity, donor cells obtained from Thy congenic mice were used for adoptive transfer. Thus, host and donor T cells could be readily distinguished by the expression of either Thy-1.2 or Thy-1.1 antigen. The results demonstrated that the majority of immunologically competent T cells present in hosts cured by adoptive therapy were of host origin. A small population of donor T cells, however, persisted long after transfer. At day 60, a time point shortly after tumor eradication had been completed, 5% of splenic T cells were of donor origin, and by day 120 this percentage had decreased to less than 2%. Functional studies performed at both time points revealed that this small number of residual donor T cells contained the subpopulation of tumor-reactive T cells present in the host. Thus, host T cells did not make a substantial contribution to the expression of the anti-tumor response and presumably have little role in either tumor eradication or the long-term maintenance of tumor immunity.

Animals↗
PubMed1979

Regulation of immune response to tumor antigen: interference with syngeneic tumor immunity by anti-IA alloantisera.

We present evidence for a role of I-A subregion-encoded determinants in syngeneic tumor immunity. In animals rendered immune to the S1509a fibrosarcoma, daily treatment with microliter quantities of antisera directed against Kk and I-Ak determinants expressed on lymphoid cells of host origin decreased the capacity for immune tumor rejection. Absorption studies revealed that anti-I-Ak antibody activity alone was sufficient for the manifestation of this effect. Furthermore, experiments utilizing F1 hybrids showed that an antiserum that was genetically unable to interact with H-2 determinants expressed on the tumor was equally effective in inhibiting tumor immunity. Suggestive evidence that the activity of this antiserum is related to interference with the generation of effector T cell function was provided by the observation that hyperimmune animals pretreated with an anti-Kk,I-Ak antiserum were no longer capable of adoptively transferring tumor immunity to naive recipients. Thus, it is possible to regulate the secondary immune response to tumor antigens by using antisera with specificity for I-A determinants expressed on cells or possibly on factors of the host lymphoid system.

Animals↗
PubMed1989

Development of antitumor reactivity in regional draining lymph nodes from tumor-immunized and tumor-bearing murine hosts.

With use of the weakly immunogenic MCA 105 tumor of the C57BL/6 mouse, the antitumor reactivity of lymphoid cells derived from the regional draining lymph nodes (RLN) of tumor-immunized and tumor-bearing mice was examined. Mice were immunized with an inoculation of viable tumor admixed with Corynebacterium parvum. Excision of tumor immunization sites within 4 days abrogated the development of systemic immunity to reject a tumor challenge. However, excision of the immunization site on day 6 did not interfere with the development of systemic antitumor immunity. In subsequent experiments, tumor immunization sites were excised on day 6 in all mice and the RLN either left intact or excised on day 6 or day 14. The development of systemic tumor immunity was severely impaired if RLN were excised on day 6, indicating the pivotal role of the RLN. Excision of the RLN on day 14 had no impact on the development of systemic immunity, thus indicating that the requirement for the RLN was time dependent. In mice bearing progressively growing tumors, lymphoid cells derived from RLN were examined for therapeutic efficacy in adoptive immunotherapy experiments. Although fresh RLN cells harvested 6 and 14 days after tumor inoculation did not demonstrate inherent therapeutic efficacy, after in vitro sensitization with irradiated tumor cells and interleukin-2, these RLN cells acquired significant antitumor activity in adoptive immunotherapy experiments. These data indicate that RLN are essential in the development of tumor immunity and may be used as a source of therapeutic effector cells for adoptive immunotherapy.

Animals↗
PubMed1977

Tumor immunity to murine plasma cell tumors. III. Detection of common and unique tumor-associated antigens on BALB/c, C3H, and NZB plasmacytomas by in vivo and in vitro induction of tumor-immune responses.

Tumor-associated antigens (TAA) were demonstrated on plasmacytomas derived from BALB/c, NZB, and C3H mouse strains, by in vivo and in vitro techniques. By immunizing the appropriate F1 hybrid mice with these tumors, it was possible to show that all the plasmacytomas expressed cross-reactive tumor-associated transplantation antigens. When cytotoxic lymphocytes (CL) were induced in vitro by the coculturing of syngeneic or F1 hybrid spleen cells with irradiated plasmacytoma cells, "shared" and "unique" plasmacytoma TAA were demonstrable. This was accomplished by inducing CL in vitro against one syngeneic plasmacytoma and assaying for lytic activity on a range of 51Cr-labeled BALB/c, NZB and C3H plasmacytoma cells in vitro. In a second in vitro assay, unlabeled plasmacytoma cells were tested for their ability to inhibit the lysis of a particular 51Cr-labeled plasmacytoma, with the use of CL induced in vitro against it. The possibility that these TAA were "self" antigens was excluded by demonstrating in the inhibition assay that they were not present on T lymphomas and spleen cells of the same strain, and that CL "autosensitized" in vitro could not significantly lyse 51Cr-labeled plasmacytoma cells in vitro. From both in vivo and in vitro studies of immunity to these tumors, it was concluded that any one plasmacytoma line possesses multiple TAA of both shared and unique types.

Animals↗
PubMed1976

The specificity of concomitant tumor immunity at large tumor volumes.

Two antigenically distinct fibrosarcomas, designated BP-8 and BP-9, induced in syngeneic C3H/HeN mice by 3,4-benzo(a)pyrene were used to study tumor-specific immunity, concomitant tumor immunity and the effect of large tumor volumes on the loss of immunological reactivity. Two groups of mice were immunized to the BP-8 tumor by amputation of growing BP-8 isografts. One group was rechallenged with the BP-8 cells, and tumor growth was not noted. Both groups of mice then received an inoculum of BP-9 cells that grew to palpable tumors to the same extent as in control mice. BP-8-immunized mice bearing progressively larger PB-9 tumors were sacrified at varying intervals after the BP-9 isograft. Tumor weight was recorded as a percentage of total body weight and viable spleen cells from these animals were tested in vitro for cytotoxicity against BP-8 and BP-9 cells in the [125I]iododeoxyuridine microcytotoxicity assay. Spleen cells from untreated mice were used as controls. The mice with growing BP-9 tumors developed an immune reaction against the tumor antigens which increased with time from initial tumor isograft and with increasing tumor size up to a definite but variable limit. Cytotoxicity to BP-9 cells rose from 18% when the BP-9 tumor was not palpable to a maximum of 77% when the tumor represented 5 to 10% of the total body weight. Cytotoxicity to BP-9 fell progressively as tumor size exceeded 15% of the total body weight and approached the 10% background cytotoxicity of control lymphocytes to BP-9 cells, when the tumor weight achieved 25% of the animal's weight. Conversely, cytotoxicity of lymphocytes against the BP-8 tumor did not vary significantly and remained about 41 to 44% over the same interval even while specific reactivity to BP-9 cells significantly decreased. In addition, with time, lymphocyte-mediated cytotoxicity to the BP-8 tumor increased from 41 to 70% if the BP-8-immunized mice had been rechallenged with antigenically identical BP-8 cells prior to the BP-9 isograft. These data suggest that loss of immunoreactivity at large tumor volumes is tumor and, presumably, antigen specific. No evidence of a generalized immune paralysis was demonstrated, since the mice always maintained immunity to the BP-8 tumor despite progressive and lethal growth of the antigenically distinct BP-9 tumor.

Animals↗