These results suggest that increased IDO activity is involved in disease progression of lung cancer, possibly through its immunosuppressive effect.

PD-L1, IDO-1, and B7-H4 are differentially expressed in human lung carcinomas and show limited co-expression. While PD-L1 and IDO-1 are associated with increased tumor-infiltrating lymphoycte and IFN-gamma stimulation, B7-H4 is not.

These findings indicate that IDO1 has the potential to participate in or contribute to the formation of new capillaries, supporting the applicability of IDO1-targeting molecular therapy in lung cancer.

An IDO1 inhibitor, epacadostat also demonstrated promising activity in combination with the PD-1 checkpoint inhibitors in other solid tumors, including melanoma, urothelial carcinoma, renal cell carcinoma, and non-small cell lung cancer

IDO-1 is commonly expressed by non-small cell lung cancers... its frequent coexpression with PD-L1 may account for the increased efficacy seen with dual blockade of PD-1/PD-L1 and IDO in clinical studies.

Results suggest that indoleamine 23-dioxygenase 1 (IDO1) and programmed cell death-ligand 1 (PD-L1) co-expression may define an aggressive form of lung adenocarcinoma.

In our study, it was found that non-small cell lung cancer-induced lung cancer cells showed a 5.22-fold increase in the IDO gene expression

expression of PD-L1, PD-L2, and IDO1 on tumor cells and density of CD8-positive tumor-infiltrating lymphocytes in early-stage lung adenocarcinoma according to histological subtype.

Indoleamine 2,3-dioxygenase regulates anti-tumor immunity in lung cancer by metabolic reprogramming of immune cells in the tumor microenvironment

IDO1 has a role in an anti-PD1-resistant lung cancer model (344SQ_R) that is different from in the parental 344SQ tumors

Results show a caspase recruitment domain-containing protein 9 (CARD9)-NF-kappa B (NF-kappaB)-IDO Dioxygenase (IDO) pathway in myeloid-derived suppressor cells (MDSCs) which can inhibit the suppressive function of MDSCs and prevent lung cancer development.