study concludes B7-H4 negatively regulates T cell-mediated antitumour immunity in nonsmall-cell lung cancer

in pulmonary adenocarcinoma presenting with SPN, nuclear membrane localization of B7-H4 within the tumor cells is associated with increased malignancy

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.

our study demonstrates a strong promoting role of B7-H4 in lung tumor growth, progression and metastasis

B7-H3 protein is expressed in the majority of NSCLCs and is associated with smoking history. High levels of B7-H3 protein have a negative prognostic impact in lung carcinomas. Coexpression of B7-H3 with PD-L1 and B7-H4 is relatively low, suggesting a nonredundant biological role of these targets.

When compared to early-stage lung adenocarcinoma, metastatic pleural adenocarcinoma possessed higher level of nuclei membranous B7-H4 and lower cytoplasmic B7-H4 expression.

The B7-H4 gene induces immune escape partly via upregulating the PD-1/Stat3 pathway in non-small cell lung cancer.

Insulin-like growth factor-1 receptor induces immunosuppression in lung cancer by upregulating B7-H4 expression through the MEK/ERK signaling pathway.

B7-H4 expression may influence the outcome of T-cell tumor cell interactions. tumor-associated macrophage induced membrane-bound B7-H4 on lung cancer cell represents a novel mechanism by which lung cancer cells evade immune recognition and destruction.