Tumor-derived immunoglobulin-like transcript 3 inhibition reshapes the immunosuppressive tumor microenvironment and potentiates programmed cell death ligand 1 blockade immunotherapy in lung adenocarcinoma.

ABSTRACT: The low response rate of current immune checkpoint inhibitors in cancer has necessitated the development of new immune targets. Survival and public databases analyses were performed to determine the clinical significance of immunoglobulin-like transcript 3 (ILT3). The impact of ILT3 and apolipoprotein E (APOE) on tumor-associated macrophage (TAM) recruitment and polarization were evaluated by transwell assay, flow cytometry (FCM), and real-time PCR, while their impact on T cell survival and cytotoxicity was detected by CFSE, apoptotic assay, FCM and ELISA. These pro-tumoural activity of (an ortholog of ILT3 in mouse) were verified in vivo models. Survival and public databases analyses revealed that high ILT3 expression was significantly associated with worse prognosis in lung adenocarcinom

SUBMITTER: Wang L 

PROVIDER: S-EPMC12008602 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature