Investigation of γδ T cell function in a novel inducible model of lung adenocarcinoma

Abstract γδ T cells have been demonstrated to both promote tumor growth/metastasis and efficiently kill cells. This dual role of has attributed their ability produce either IL-17 (γδT17) or IFNγ (γδT1), the former being associated with progression latter anti-tumor activity. cell function is influenced by multiple factors, including recognition stress-induced ligands, as well cytokines chemokines. However, specific signals that lead selective activation γδT17 γδT1 subsets in different cancers remains unclear. Here, we explored these questions using a novel inducible mouse model Kras-driven lung adenocarcinoma without co-mutation Stk11, master regulator metabolic pathways. Preliminary characterization this revealed Kras G12D/Stk11 fl/flmice exhibited significantly greater morbidity than G12Dmice. While leukocyte numbers did not differ between G12Dand fl/flmice, noted increased frequency γδT17, but γδT1, fl/fllungs. Interestingly, was due Vγ1 Vγ6, Vγ4, suggesting expansion subsets. To examine potential for butyrophilins models, assessed butyrophilin gene expression qPCR. analysis Btnl1, Btnl2, Btnl9 G12Dlungs mice compared controls. Together, results suggest shed new light on how interaction microenvironment affects disease pathogenesis.