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  • CYTOKINE  (2)
  • cytokines  (2)
  • ANTI-ERBB-2 ANTIBODY  (1)
Keywords
  • 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: 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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  • 3
    Keywords: CELLS ; IN-VIVO ; GENE ; GENE-EXPRESSION ; MICE ; IFN-GAMMA ; MOUSE ; CD4(+) T-CELLS ; CYTOKINE ; DEFICIENCY ; IL-7 ; HOMEOSTATIC PROLIFERATION ; GUT ; INTESTINAL EPITHELIAL-CELLS ; Commensal microflora ; Intestinal epithelial cells
    Abstract: IL-7 is a major regulator of lymphocyte homeostasis; however, little is known about the mechanisms that regulate IL-7 production. To study Il7 gene regulation in vivo, we generated a novel IL-7-reporter mouse, which allows the non-invasive quantification of Il7 gene activity in live mice and, additionally, the simultaneous activation/inactivation of target genes in IL-7-producing cells. With these IL-7-reporter mice, we identify thymus, skin and intestine as major sources of IL-7 in vivo. Importantly, we show that IFN-gamma and the commensal microflora promote steady-state IL-7 production in the intestine. Furthermore, we demonstrate that the blockade of IFN-gamma signaling in intestinal epithelial cells strongly reduces their IFN-gamma-driven IL-7 production. In summary, our data suggest a feedback loop in which commensal bacteria drive IFN-gamma production by lymphocytes, which in turn promotes epithelial cell IL-7 production and the survival of IL-7-dependent lymphocytes
    Type of Publication: Journal article published
    PubMed ID: 20690180
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