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  • tumor  (4)
  • cytokines  (2)
  • 1
    Keywords: CANCER ; CELLS ; ENDOTHELIAL-CELLS ; GROWTH ; tumor ; TUMOR-CELLS ; Germany ; IN-VIVO ; TUMORS ; IFN-GAMMA ; T-CELLS ; fibroblasts ; MOLECULE ; cytokines ; CANCER-CELLS ; INTERFERON-GAMMA ; adoptive immunotherapy ; MALIGNANT-CELLS ; TUMOR-GROWTH ; endothelial cells ; SOLID TUMORS ; ESTABLISHED TUMORS ; FAS LIGAND ; NECROSIS-FACTOR ; EFFECTOR T-CELLS ; MAMMARY-CARCINOMA
    Abstract: For decades it has been assumed that T cells reject tumors essentially by direct killing. However, solid tumors are composed of malignant cells and a variety of different nonmalignant cells, referred to as tumor stroma. Stromal cells, such as endothelial cells, fibroblasts and inflammatory cells, often support tumor growth. Here, we discuss new findings showing that the tumor stroma is an important target during T-cell-mediated tumor rejection. Cytotoxic molecules and cytokines produced by T cells inhibit or destroy the stromal 'infrastructure', thereby withdrawing essential resources and leading to tumor infarction and subsequent T-cell-mediated elimination of residual tumor cells. These findings are important for the development of more effective and specific immunotherapies for cancer
    Type of Publication: Journal article published
    PubMed ID: 15882610
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  • 2
    Keywords: PEPTIDE ; EXPRESSION ; tumor ; DENDRITIC CELLS ; TOLERANCE ; MELANOMA-CELLS ; thymic epithelium ; ALPHA-CHAIN ; PERIPHERAL-TISSUE ANTIGENS ; MEDULLARY EPITHELIAL-CELLS
    Abstract: Immunity to tumor differentiation antigens, such as melanoma antigen recognized by T cells 1 (MART-1), has been comprehensively studied. Intriguingly, CD8(+) T cells specific for the MART-1(26(27)-35) epitope in the context of HLA-A0201 are about 100 times more abundant compared with T cells specific for other tumor-associated antigens. Moreover, MART-1-specific CD8(+) T cells show a highly biased usage of the Valpha-region gene TRAV12-2. Here, we provide independent support for this notion, by showing that the combinatorial pairing of different TCRalpha- and TCRbeta- chains derived from HLA-A2-MART-1(26-35) -specific CD8(+) T-cell clones is unusually permissive in conferring MART-1 specificity, provided the CDR1alpha TRAV12-2 region is used. Whether TCR bias alone accounts for the unusual abundance of HLA-A2-MART-1(26-35) -specific CD8(+) T cells has remained conjectural. Here, we provide an alternative explanation: misinitiated transcription of the MART-1 gene resulting in truncated mRNA isoforms leads to lack of promiscuous transcription of the MART-1(26-35) epitope in human medullary thymic epithelial cells and, consequently, evasion of central self-tolerance toward this epitope. Thus, biased TCR usage and leaky central tolerance might act in an independent and additive manner to confer high frequency of MART-1(26-35) -specific CD8(+) T cells.
    Type of Publication: Journal article published
    PubMed ID: 24846220
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  • 3
    Keywords: CELLS ; tumor ; TUMOR-CELLS ; IN-VIVO ; TUMORS ; MICE ; RESPONSES ; CUTTING EDGE ; IFN-GAMMA ; ANTIGEN ; T-CELLS ; TOLERANCE ; bone marrow ; RECOGNITION ; LYMPHOCYTES ; IMMUNITY ; REJECTION ; CROSS-PRESENTATION ; EXOGENOUS ANTIGEN ; NONHEMATOPOIETIC CELLS ; PRESENTING CELLS
    Abstract: CD8(+) effector T cells recognize malignant cells by monitoring their surface for the presence of tumor-derived-peptides bound to MHC class I molecules. In addition, tumor-derived-Ags can be cross-presented to CD8(+) effector T cells by APCs. IFN-gamma production by CD8(+) T cells is often critical for tumor rejection. However, it remained unclear whether 1) CD8(+) T cells secrete IFN-gamma in response to Ag recognition on tumor cells or APCs and 2) whether IFN-gamma mediates its antitumor effect by acting on host or tumor cells. We show in this study that CD8(+) effector T cells can reject tumors in bone marrow- chimeric mice incapable of cross-presenting Ag by bone marrow- derived APCs and that tumor rejection required host cells to express IFN-gammaR. Together, CD8(+) effector T cells recognize Ag directly on tumor cells, and this recognition is sufficient to reject tumors by IFN-gamma acting on host cells
    Type of Publication: Journal article published
    PubMed ID: 12707316
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  • 4
    Keywords: CANCER ; CELLS ; GROWTH ; PROTECTION ; tumor ; carcinoma ; CELL ; MODEL ; TUMORS ; MICE ; PATIENT ; DNA ; IFN-GAMMA ; T cell ; T cells ; T-CELL ; T-CELLS ; BREAST ; breast cancer ; BREAST-CANCER ; cytokines ; antibodies ; antibody ; SWEDEN ; SURFACE ; VACCINE ; CANCER-PATIENTS ; CARCINOMAS ; CD8(+) ; immune response ; IMMUNE-RESPONSE ; IMMUNITY ; T-LYMPHOCYTES ; vaccination ; REJECTION ; CANCER PATIENTS ; CTL ; INTERFERON-GAMMA ; EFFECTOR ; GM-CSF ; HER-2/neu ; IMMUNIZATION ; ABSENCE ; CYTOKINE ; tumor immunity ; ANTI-ERBB-2 ANTIBODY ; anti-tumor immunity ; DNA vaccine ; ERBB-2 DNA ; PROTOONCOGENE
    Abstract: HER-2/neu (HER-2) is a cell surface proto-oncogene that is often overexpressed in carcinomas. Passive administration of anti-HER-2 antibodies in breast cancer patients has achieved promising results, but less is known about the role of antibodies in active immunization. We asked whether B cells/ antibodies are needed for tumor immunity induced by plasmid (HER-2 and GM-CSF) immunization. HER-2 specific tumor immunity relied completely on both CD4(+) and CD8(+) T cells. IFN-gamma, and to a lesser extent IL-4, seemed to be crucial cytokines during tumor rejection. Protection was associated with production of anti-HER-2 IgG antibodies in B cell competent mice. After immunization, however, B cell-deficient mice rejected HER-2-expressing tumors as efficiently as control littermates. We conclude that T cells are the main effector cells in DNA vaccine induced immunity against HER-2 and that anti HER-2 antibodies are not necessary to elicit a protective anti tumor immune response in this model. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14750178
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