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The role of STAT3 in T-cell responses during the development of NSCLC

STAT (Signal transducer and activator of transcription) 3 is activated via phosphorylation induced by pro-inflammatory cytokines and growth factors and promotes tumorigenesis by regulating cellular senescence, proliferation and apoptosis. STAT3 is also important for the differentiation of both T regulatory (Treg) cells which suppress anti-tumor immune responses and T helper 17 cells, a T-cell subtype expanded in lung ADC (adenocarcinoma). However, the role of STAT3 in tumor-infiltrating lymphocytes in NSCLC (non-small cell lung cancer) is largely unknown. Here, we investigated the functional effects of STAT3 inactivation in T cells in a murine model of lung ADC. We found that STAT3ΔCD4 mice showed increased lung tumor growth as compared to control littermates. This phenotype was found associated with impaired lung CD8+ cytotoxic T-cell functions indicated by a reduced production of IFNγ (Interferon γ) and TNFα (Tumor necrosis factor α) in the absence of STAT3. Furthermore, we discovered that lung Tregs of STAT3ΔCD4 mice preferentially express PD1 (Programmed cell Death protein 1) while there is an increase in PD-L1+ (Programmed Death-Ligand 1) EpCAM+ (Epithelial Cell Adhesion Molecule) cells in the absence of STAT3. This indicates a regulation of the PD1/PD-L1 signaling axis in STAT3ΔCD4 mice that could induce the Treg inhibitory functions and the adaption to an immunosuppressive tumor microenvironment during the development of NSCLC.