Inhibitory Fcγ receptor deletion enhances CD8 T cell stemness increasing anti-PD-1 therapy responsiveness against glioblastoma.

ABSTRACT:

Background

Certain cancers present challenges for treatment because they are resistant to immune checkpoint blockade (ICB), attributed to low tumor mutational burden and the absence of T cell-inflamed features. Among these, glioblastoma (GBM) is notoriously resistant to ICB. To overcome this resistance, the identification of T cells with heightened stemness marked by T-cell factor 1 (TCF1) expression has gained attention. Several studies have explored ways to preserve stem-like T cells and prevent terminal exhaustion. In this study, we investigate a target that triggers stem-like properties in CD8 T cells to enhance the response to ICB in a murine GBM model.

Methods

Using Fcgr2b^-/- mice and a murine GL261 GBM model, we confirmed the efficacy of anti-program

SUBMITTER: Ku KB 

PROVIDER: S-EPMC11529582 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature