Lung adenocarcinoma-derived IFN-γ promotes growth by modulating CD8+ T cell production of CCR5 chemokines.

ABSTRACT: Because the lung is a mucosal barrier organ with a unique immunologic environment, mechanisms of immunoregulation in lung cancer may differ from those of other malignancies. Consistent with this notion, we found that CD8+ T cells played a paradoxical role in facilitating, rather than ameliorating, the growth of multiple lung adenocarcinoma models. These included spontaneous, carcinogen-induced, and transplantable tumor cell line models. Specifically, we found that CD8+ T cells promoted homing of CD4+Foxp3+ Tregs to the tumor bed by increasing the levels of CCR5 chemokines in the tumor microenvironment in an IFN-γ- and TNF-α-dependent manner. Contrary to their canonical role, these Th1 cytokines contributed to accelerated growth of murine lung adenocarcinomas, while suppressing the growth o

SUBMITTER: Kratzmeier C 

PROVIDER: S-EPMC12404755 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature