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

The B7-H4 gene induces immune escape partly via upregulating the PD-1/Stat3 pathway in non-small cell lung cancer. Hum Immunol. 2020 Feb 26;: Authors: Yuan L, Ye J, Fan D Abstract Non-small cell lung cancer (NSCLC) is associated with high mortality rates worldwide. The costimulatory molecule, B7-H4, a member of the B7 family, plays an important role in immune regulation, mainly by inhibiting the proliferation of T cells to achieve a negative regulatory T cell immune response. The mechanism of action of B7-H4 in non-small cell lung cancer is unknown at present. Tumor tissues from 71 patients subjected to radical pneumonectomy were examined, along with NSCLC cells and BALB/c mice. Among the 71 NSCLC cases, overall and recurrence-free survival rates were significantly lower in those displaying high B7-H4 expression. Mechanistic analyses showed that B7-H4 promoted the growth and metastasis of non-small cell lung cancer tumor tissues in mice through effects on CD8+ T cell apoptosis. Data from western blot experiments further suggested that B7-H4 induced CD8+ T cell death, both in vitro and in vivo, and affecting the PD-1/Stat3 pathway and promoting immune escape of tumor cells. Our collective findings support the potential utility of B7-H4 gene expression as a marker of NSCLC prognosis and provide a novel strategy for targeted therapy. PMID: 32113654 [PubMed - as supplied by publisher]
Source: Human Immunology - Category: Allergy & Immunology Authors: Tags: Hum Immunol Source Type: research