Deciphering the potential role of PGRN in regulating CD8⁺ T cell antitumor immunity.

ABSTRACT: A key factor contributing to resistance in immune checkpoint blockade (ICB) therapies is CD8⁺ T-cell tolerance in the tumor microenvironment (TME), partly resulting from upregulating coinhibitory receptors. Here, we describe the role of PGRN as a coinhibitory molecule that modulates the antitumor response of CD8⁺ T cells, thus presenting a novel immunosuppressive target for lung cancer. The in vivo subcutaneous transplanted lung cancer model showed that PGRN expression was elevated on CD8⁺ T cells that infiltrated transplanted lung cancers. Furthermore, PGRN deficiency was found to specifically encourage the infiltration of CD8⁺ T cells, enhance their proliferation, migration, and activation, and resist apoptosis, ultimately inhibiting tumor grow

SUBMITTER: Zhang W 

PROVIDER: S-EPMC11094002 | biostudies-literature | 2024 May

REPOSITORIES: biostudies-literature