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    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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