期刊
CANCER CELL
卷 18, 期 2, 页码 160-170出版社
CELL PRESS
DOI: 10.1016/j.ccr.2010.06.014
关键词
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资金
- U S National Institutes of Health [AI062026, CA115540, CA97296, P50 CA125183]
- National Key Basic Research Program [2006CB910901]
- Natural Science Foundation [C0302050102]
- Korean Government (MOEHRD) [KRF-2007-013-E00017]
- Inje University
- Korea Science and Engineering Foundation (KOSEF) [R13-2007-023-00000-0]
- [T32AI007090]
Anti-HER2/neu antibody therapy is reported to mediate tumor regression by interrupting oncogenic signals and/or inducing FcR-mediated cytotoxicity. Here, we demonstrate that the mechanisms of tumor regression by this therapy also require the adaptive immune response. Activation of innate immunity and T cells, initiated by antibody treatment, was necessary. Intriguingly, the addition of chemotherapeutic drugs, although capable of enhancing the reduction of tumor burden, could abrogate antibody-initiated immunity leading to decreased resistance to rechallenge or earlier relapse. Increased influx of both innate and adaptive immune cells into the tumor microenvironment by a selected immunotherapy further enhanced subsequent antibody-induced immunity, leading to increased tumor eradication and resistance to rechallenge. This study proposes a model and strategy for anti-HER2/neu antibody-mediated tumor clearance.
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