Author/Authors :
Park، نويسنده , , SaeGwang and Jiang، نويسنده , , Zhujun and Mortenson، نويسنده , , Eric D. and Deng، نويسنده , , Liufu and Radkevich-Brown، نويسنده , , Olga and Yang، نويسنده , , Xuanming and Sattar، نويسنده , , Husain and Wang، نويسنده , , Yang and Brown، نويسنده , , Nicholas K. and Greene، نويسنده , , Mark and Liu، نويسنده , , Yang and Tang، نويسنده , , Jie and Wang، نويسنده , , Shengdian and Fu، نويسنده , , Yang-Xin، نويسنده ,
Abstract :
Summary
ER2/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.
