Myeloid STAT3 Promotes Lung Tumorigenesis by Transforming Tumor Immunosurveillance into Tumor-Promoting Inflammation.

ABSTRACT: One of the most fundamental and challenging questions in the cancer field is how immunity in patients with cancer is transformed from tumor immunosurveillance to tumor-promoting inflammation. Here, we identify the transcription factor STAT3 as the culprit responsible for this pathogenic event in lung cancer development. We found that antitumor type 1 CD4⁺ T-helper (Th1) cells and CD8⁺ T cells were directly counter balanced in lung cancer development with tumor-promoting myeloid-derived suppressor cells (MDSCs) and suppressive macrophages, and that activation of STAT3 in MDSCs and macrophages promoted tumorigenesis through pulmonary recruitment and increased resistance of suppressive cells to CD8⁺ T cells, enhancement of cytotoxicity toward CD4⁺ a

SUBMITTER: Zhou J 

PROVIDER: S-EPMC5334370 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature