These results suggest that IL-10, TNF-alpha and TGF-beta1 gene polymorphisms may affect host susceptibility to lung cancer and the outcome of the patients.

interaction between lung cancer cells and CD4(+) T cells induces DNMT expression and IFNG promoter hypermethylation in CD4(+) T cell, which may serve as an important mechanism of tumor-induced immunosuppression.

a decrease in PTEN facilitates ROS/SHP2 signaling, causing lung cancer cells to become unresponsive to IFN-gamma

IFNgamma+874 A/T and IL10-1082 G/G gene polymorphisms were found to be significantly associated with non-small cell lung cancer with 1.56- and 1.68-fold disease risk, respectively.

findings provide evidence for crosstalk between JAK2-STAT1 and PI3K-AKT pathways in response to IFN-gamma in lung adenocarcinoma and have implications for the design of combinatorial targeted therapy and immunotherapy for the treatment of lung adenocarcinoma

Absence of PD-L1 expression on tumor cells in the context of an activated immune infiltrate may indicate impaired IFNgamma signaling in non-small cell lung cancer/

IFN-gamma production from lung resident NK cells is a key response in the natural resistance to the experimental lung metastasis of NK cell-resistant tumor cells.

Umbelliprenin induced production of IFN-gamma and TNF-alpha, and reduced IL-10, IL-4, Foxp3 and TGF-beta in a mouse model of lung cancer.

the protective effect on metastasis was lost upon patrolling monocyte or NK cell depletion, IL15 neutralization, or IFNgamma ablation. The combined analysis of these approaches allowed us to establish a hierarchy in which patrolling monocytes, making IL15 in response to primary tumors, activate NK cells and IFNg production that then inhibit lung metastasis formation.