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
Deep Link:
http://www.dkfz.de/cgi-bin/sel?http://www.dkfz.de/PublicationManager/Show/ShowJournal.aspx%3fpublishedId=1397
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