It is shown that KRASG12D mutations in lung epithelium drive proliferation of resident, embryonically-derived alveolar macrophages, which then promote tumor cell proliferation and protection from ferroptosis, leading to tumor progression.
Non-small cell lung cancer (NSCLC), particularly oncogene-driven subtypes, remains a leading cause of cancer-related mortality, underscoring the urgent need for novel immunotherapies that effectively target the tumor immune microenvironment (TIME). The interleukin-9 receptor (IL-9R) signaling pathway is understud...
Jilu Zhang, M. Kaplan· Journal of Immunology· 0 citations
A model in which tumor-specific type 17 T cells directly reprogram cancer cell epigenetics through IL-26 is supported, reshaping the tumor immune microenvironment to promote immune evasion and immune evasion.
T. Itoh, R. Hatano, Y. Hasegawa et al.· Nature Communications· 0 citations
It is demonstrated that CD4+ T cells accumulate in tumor-free lungs and promote tumor metastasis in mouse models, and STAT3 and IL-17 in CD4+ T cells therefore are important for pre-metastatic niche formation and metastasis.
Maciej Kujawski, Antons Martincuks, M. Song et al.· Journal for ImmunoTherapy of...· 0 citations
Tumor Immunology: Cellular Responses and Tumor Microevironment (TIME) shows that tumor-intrinsic Stk11 loss in lung adenocarcinoma is associated with an expansion of lung gdT17 cells and supports a model in which these pro-tumor cells are recruited to the KS mouse lung via a CXCL16-CXCR6 axis.
Katherine J Horrigan, Joshua M. Ragusa, Somen K. Mistri et al.· Journal of Immunology· 0 citations
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