| First Author | Jin C | Year | 2019 |
| Journal | Cell | Volume | 176 |
| Issue | 5 | Pages | 998-1013.e16 |
| PubMed ID | 30712876 | Mgi Jnum | J:359967 |
| Mgi Id | MGI:7791028 | Doi | 10.1016/j.cell.2018.12.040 |
| Citation | Jin C, et al. (2019) Commensal Microbiota Promote Lung Cancer Development via gammadelta T Cells. Cell 176(5):998-1013.e16 |
| abstractText | 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 gammadelta 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-1beta and IL-23 production from myeloid cells, inducing proliferation and activation of Vgamma6(+)Vdelta1(+) gammadelta 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. |
