Cell:共生菌群通过γδ T细胞促进肺癌发展
创作:aluba 审核:aluba 2019年02月02日
  • 共生菌群促进肺腺癌小鼠模型的肿瘤生长,而肺部肿瘤的发展与肺部菌群改变及促炎症因子表达增加相关;
  • 抗生素处理普通小鼠或无菌小鼠后,肺腺癌的发展受到抑制;
  • 共生菌群可通过激活Myd88通路,刺激髓系细胞产生IL-1β及IL-23,从而促进肺部可产生IL-17的γδ T细胞(主要是Vγ6+ Vδ1+ T细胞)的增殖与活化;
  • 菌群诱导的γδ T细胞可促进中性粒细胞浸润,并可促进肺部肿瘤发展;
  • 与肺部肿瘤相关的γδ T细胞有着独特的转录谱。
主编推荐语
aluba
肺癌与慢性炎症密切相关,肺部菌群在其中的作用尚未明确。Cell上发表的一项最新研究发现,无菌小鼠的肺癌进展受到抑制,而肺部共生菌群通过激活肺部的γδ T细胞,促进了肺腺癌的发生发展。
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Cell [IF:41.582]

Commensal Microbiota Promote Lung Cancer Development via γδ T Cells

共生菌群通过γδ T细胞促进肺癌发展

10.1016/j.cell.2018.12.040

2019-01-31, Article

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Lung cancer is closely associated with chronic inflammation, but the causes of inflammation and the specific immune mediators have not been fully elucidated. The lung is a mucosal tissue colonized by a diverse bacterial community, and pulmonary infections commonly present in lung cancer patients are linked to clinical outcomes. Here, we provide evidence that local microbiota provoke inflammation associated with lung adenocarcinoma by activating lung-resident gd T cells. Germ-free or antibiotictreated mice were significantly protected from lung cancer development induced by Kras mutation and p53 loss. Mechanistically, commensal bacteria stimulated Myd88-dependent IL-1b and IL-23 production from myeloid cells, inducing proliferation and activation of Vg6+ Vd1+ gd T cells that produced IL-17 and other effector molecules to promote inflammation and tumor cell proliferation. Our findings clearly link local microbiota-immune crosstalk to lung tumor development and thereby define key cellular and molecular mediators that may serve as effective targets in lung cancer intervention.

First Authors:
Chengcheng Jin

Correspondence Authors:
Tyler Jacks

All Authors:
Chengcheng Jin,Georgia K Lagoudas,Chen Zhao,Susan Bullman,Arjun Bhutkar,Bo Hu,Samuel Ameh,Demi Sandel,Xu Sue Liang,Sarah Mazzilli,Mark T Whary,Matthew Meyerson,Ronald Germain,Paul C Blainey,James G Fox,Tyler Jacks

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