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董晨Science后发Immunity文

2018-12-07 03:37:25

董晨Science后发Immunity文章 解析肿瘤免疫机制

生物通报道,来自M.D Anderson Cancer Center免疫学系的科学家董晨教授今年8月曾在Science版上发表了辅助T细胞发育调控方面的研究进展,近期他的研究小组再度取得新进展,这次他们发现辅助T细胞17对肿瘤免疫具有重要的活性,相关成果文章T Helper 17 Cells Promote Cytotoxic T Cell Activation in Tumor Immunity发表在权威期刊,《Immunity》上。

文章通讯作者是M.D Anderson Cancer Center免疫系的董晨教授,早年毕业于武汉大学,赴美留学时师从美国科学院院士Max Cooper教授(发现B细胞的科学家),董晨教授现任M.D Anderson Cancer Center免疫系正教授。

上次发表的Science文章主要解释了Bcl6转录因子对辅助T细胞生长发育的调控作用。

(了解更多请点击专访文章:专访正教授董晨开启免疫功能的新通路)

本次的《Immunity》文章主要解析辅助T细胞17(T Helper 17 Cells)可促进细胞毒性T细胞激活发挥肿瘤免疫功能。

辅助T细胞17(T Helper 17 Cells,简称,Th 17)是一种新发现的辅助T细胞亚型,主要分泌白细胞介素17,Th 17被发现在自体免疫与炎症的发生过程中发挥重要的作用,目前,研究发现,Th17在肿瘤组织中广泛存在。然而,关于Th17在肿瘤组织中的功能却一无所知。

董晨教授研究组研究发现,白细胞介素17(interleukin-17A,简称IL-17A)缺陷的小鼠更易发生肺黑色素瘤(一种癌症)。如果,对小鼠采取T细胞疗法,用分泌IL-17A的T细胞治疗可有效阻止肿瘤的发生。更重要的,在IL-17A的辅助下,Th17细胞表现出比Th1细胞更强的治疗功效。

更让人意外的是,使用Th17细胞治疗可有效激活肿瘤特异性的CD8+T细胞,CD8+T细胞是抗肿瘤的必须细胞。Th17细胞能召集树突细胞进入肿瘤组织,并且能使得CD8α+树突细胞聚集到肿瘤组织中。

此外,Th17细胞激活肿瘤组织的趋化因子CCL20。总的来说,Th17细胞可有效促进肿瘤特异性的CD8+T细胞的活性。

这些新发现,为抗肿瘤免疫治疗带来新的视野。

(生物通 张欢)

生物通推荐原文检索

T Helper 17 Cells Promote Cytotoxic T Cell Activation in Tumor Immunity

Natalia Martin-Orozco1, Pawel Muranski4, Yeonseok Chung1, Xuexian O. Yang1, Tomohide Yamazaki1, Sijie Lu2, Patrick Hwu3, Nicholas P. Restifo4, Willem W. Overwijk3 and Chen Dong1, ,

1 Department of Immunology, MD Anderson Cancer Center, Houston, TX 77030, USA

2 Department of Stem Cell Transplantation and Cell Therapy, MD Anderson Cancer Center, Houston, TX 77030, USA

3 Department of Melanoma Medical Oncology, MD Anderson Cancer Center, Houston, TX 77030, USA

4 National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA

【Summary】

Although T helper 17 (Th17) cells have been found in tumor tissues, their function in cancer immunity is unclear. We found that interleukin-17A (IL-17A)-deficient mice were more susceptible to developing lung melanoma. Conversely, adoptive T cell therapy with tumor-specific Th17 cells prevented tumor development. Importantly, the Th17 cells retained their cytokine signature and exhibited stronger therapeutic efficacy than Th1 cells. Unexpectedly, therapy using Th17 cells elicited a remarkable activation of tumor-specific CD8+ T cells, which were necessary for the antitumor effect. Th17 cells promoted dendritic cell recruitment into the tumor tissues and in draining lymph nodes increased CD8α+ dendritic cells containing tumor material. Moreover, Th17 cells promoted CCL20 chemokine production by tumor tissues, and tumor-bearing CCR6-deficient mice did not respond to Th17 cell therapy. Thus, Th17 cells elicited a protective inflammation that promotes the activation of tumor-specific CD8+ T cells. These findings have important implications in antitumor immunotherapies.

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