STAT3 in Tumor-Associated Myeloid Cells: Multitasking to Disrupt Immunity.

STAT3 in Tumor-Associated Myeloid Cells: Multitasking to Disrupt Immunity.
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DOI:
10.3390/ijms19061803
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发表时间:
2018-06-19
影响因子:
5.6
通讯作者:
Kortylewski M
Kortylewski M
中科院分区:
生物学2区
文献类型:
--
作者:
Su YL;Banerjee S;White SV;Kortylewski M

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髓样免疫细胞,如树突状细胞、单核细胞和巨噬细胞,在免疫应答的产生中起核心作用,因此经常被肿瘤禁用或甚至劫持。肿瘤相关骨髓细胞的这些新的致耐受性活性由致癌转录因子、信号转导子和转录激活子3(STAT3)控制。STAT3通过损害抗原呈递和减少免疫刺激分子的产生,同时增加致耐受性介质的释放,从而减少先天性和适应性抗肿瘤免疫,从而确保肿瘤逃避免疫检测。肿瘤相关的骨髓细胞和STAT3信号在这个隔室现在通常被认为是一个有吸引力的细胞靶点,用于提高标准疗法和免疫疗法的疗效。在此,我们回顾了STAT3信号在这种免疫细胞室中的重要性和功能复杂性以及癌症治疗的潜在策略。
Myeloid immune cells, such as dendritic cells, monocytes, and macrophages, play a central role in the generation of immune responses and thus are often either disabled or even hijacked by tumors. These new tolerogenic activities of tumor-associated myeloid cells are controlled by an oncogenic transcription factor, signal transducer and activator of transcription 3 (STAT3). STAT3 multitasks to ensure tumors escape immune detection by impairing antigen presentation and reducing production of immunostimulatory molecules while augmenting the release of tolerogenic mediators, thereby reducing innate and adaptive antitumor immunity. Tumor-associated myeloid cells and STAT3 signaling in this compartment are now commonly recognized as an attractive cellular target for improving efficacy of standard therapies and immunotherapies. Hereby, we review the importance and functional complexity of STAT3 signaling in this immune cell compartment as well as potential strategies for cancer therapy.
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