Commensal Microbiota Promote Lung Cancer Development via γδ T Cells
By C. Jin, G. Lagoudas, Chen Zhao, S. Bullman, A. Bhutkar, Bo Hu, Samuel Ameh, Demi A. Sandel, X. Liang, S. Mazzilli and 6 more. Cell, 2019
838 citations recorded by the source corpus.
Summary 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 γδ T cells. Germ-free or antibiotic-treated mice were significantly protected from lung cancer development induced by Kras mutation and p53 loss. Mechanistically, commensal bacteria stimulated Myd88-dependent IL-1β and IL-23 production from myeloid cells, inducing proliferation and activation of Vγ6+Vδ1+ γδ 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.
Subfields: Food Science, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/a1be9fccee70c55e419de70fb43c5ef9e476c445
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Citations in the corpus
- The microbiome and human cancer (2021, background): “1016/ S1470-2045(18)30952-5; pmid: 30712808”
- Hallmarks of Cancer: New Dimensions. (2022, background): “Microbiota have been similarly detected in genetically engineered de novo mouse models of lung and pancreas cancer, and their absence in germ-free mice and/or their abrogation with antibiotics can demonstrably impair tumorigenesis, functionally implicating the tumor microbiome as an enabler of tumor”