کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2107525 | 1083683 | 2010 | 11 صفحه PDF | دانلود رایگان |
SummaryAnti-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.
► The tumor regression by anti-HER2/neu antibody is T cell-dependent
► FcR-dependent stress by antibody is required to prime adaptive immune cells
► Some chemotherapy drugs could abrogate antibody-mediated immunity
► A selected immunotherapy could further enhance antibody-mediated immunity
Journal: - Volume 18, Issue 2, 17 August 2010, Pages 160–170