时间：14:00 - 15:00

地点：数学高等研究院报告厅

组织者：阮勇斌，黄德力，印焘， 宋海，周家耀

报告人：印焘 Tao Yin（浙江大学生命科学研究院）

摘要：Anti-cancer immunotherapies have demonstrated remarkable success against multiple solid tumors; however, for many patients, efficacy remains modest and temporary due to primary and/or acquired resistance. In recent years, we have sought to identify new mechanisms of immune suppression in the tumor microenvironment. For instance, while investigating novel suppressive mechanisms in melanoma, we discovered that nerve growth factor (NGF) mediates both melanoma cell-intrinsic and -extrinsic immunosuppression. In melanoma cells, autocrine NGF engages TrkA receptor, leading to desensitization of IFN-g signaling, and subsequent exclusion of T and NK cells. In parallel, paracrine NGF suppresses TCR signaling and effector function of T cells. Genetic or pharmacological targeting of NGF sensitizes melanoma to immune checkpoint blockade (ICB) therapy. Together, these findings reveal a comprehensive mechanism by which the NGF-TrkA axis suppresses anti-tumor T cell immunity, thereby providing a novel therapeutic strategy for immunotherapy.