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首页> 外文期刊>Cancer research: The official organ of the American Association for Cancer Research, Inc >Immunity to murine prostatic tumors: continuous provision of T-cell help prevents CD8 T-cell tolerance and activates tumor-infiltrating dendritic cells.
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Immunity to murine prostatic tumors: continuous provision of T-cell help prevents CD8 T-cell tolerance and activates tumor-infiltrating dendritic cells.

机译：对鼠类前列腺肿瘤具有免疫力：持续提供T细胞有助于防止CD8 T细胞耐受并激活肿瘤浸润性树突状细胞。

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摘要

We reported previously that tumor-specific CD8(+) T cells (TcR-I) become tolerant in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model. In this study, we show that CD4(+) TcR transgenic (TcR-II) T cells transferred into TRAMP mice became activated in lymph nodes, trafficked to the prostate, and initially functioned as T(H)1 cells. Although a single cotransfer of TcR-II cells delayed TcR-I cell tolerization, repeated transfer of TcR-II cells was required to prevent TcR-I cell tolerization and significantly slowed progression of TRAMP prostate tumors. After transfer of TcR-II cells, dendritic cells within the tumor expressed higher levels of costimulatory molecules and displayed an enhanced ability to stimulate proliferation of naive T cells. Blockade of CD40-CD40L interactions during TcR-II transfer resulted in a profound reduction in dendritic cell stimulatory capacity and a partial loss of TcR-I effector functions and tumor immunity. These data show that sustained provision of activated tumor-specific CD4(+) T cells alters the immunosuppressive tumor microenvironment, ultimately leading to the control of tumor growth. These findings will assist in the design of more effective immunotherapeutic approaches for cancer.
机译：我们先前报道肿瘤特异性CD8（+）T细胞（TcR-1）在小鼠前列腺（TRAMP）模型的转基因腺癌​​中变得耐受。在这项研究中，我们表明转移到TRAMP小鼠中的CD4（+）TcR转基因（TcR-II）T细胞在淋巴结中被激活，运到前列腺，最初起T（H）1细胞的作用。尽管单次共转移TcR-II细胞可延迟TcR-I细胞耐受，但仍需要重复转移TcR-II细胞以防止TcR-I细胞耐受并显着减慢TRAMP前列腺肿瘤的进展。转移TcR-II细胞后，肿瘤内的树突状细胞表达更高水平的共刺激分子，并显示出增强的刺激天然T细胞增殖的能力。在TcR-II转移过程中CD40-CD40L相互作用的阻断导致树突状细胞的刺激能力大大降低，TcR-I效应子功能和肿瘤免疫力部分丧失。这些数据表明，持续提供活化的肿瘤特异性CD4（+）T细胞会改变免疫抑制性肿瘤微环境，最终导致对肿瘤生长的控制。这些发现将有助于设计更有效的癌症免疫疗法。

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