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CD4+ T cell-mediated HER-2/neu-specific tumor rejection in the absence of B cells

✍ Scribed by Jan Alvar Lindencrona; Susanne Preiss; Thomas Kammertoens; Thomas Schüler; Marie Piechocki; Wei-Zen Wei; Barbara Seliger; Thomas Blankenstein; Rolf Kiessling

Publisher
John Wiley and Sons
Year
2003
Tongue
French
Weight
134 KB
Volume
109
Category
Article
ISSN
0020-7136

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✦ Synopsis

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‐γ, 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. © 2003 Wiley‐Liss, Inc.

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## Abstract The development of autochtonous mammary tumors in __HER‐2/neu__ transgenic mice is facilitated by immune tolerance to the __neu‐__transgene. However, appropriate vaccination strategies can initiate immune system‐mediated antitumor response by a process that requires IFN‐γ. We investigat