讲座简介：
The immune system plays essential roles in tumorigenesis, tumor progression and metastasis. We found that mice with T cell-specific deletion of the mediator subunit Med23 (Med23-deficient) spontaneously developed AT2 cell-originated lung adenocarcinomas with elevated mutation rate in oncogenes. Increased AT2 cells bearing oxidative stress and oxidative DNA damages were detected prior to the formation of lung adenocarcinoma. The major immune defect accompanying tumor development in Med23-deficient mice was mapped to a dramatic decrease of tissue-resident memory T cells (CD103+ T cell) which displayed close contacts with AT2 cells in situ. CD103+ T cells exhibited the ability of eradicating oxidative-damage-bearing AT2 cells as well as KRASG12D-driven carcinomas in the lung. In vitro co-culture system proved that CD103+ T cells induced cell-death to target cells under augmented oxidative stress. Our study establishes that CD103+ T cells play a vital role in surveilling tissue somatic cells under oxidative stress to prevent tumorigenesis and supports that Med23 is the key regulator of CD103+ T cell generation.
主讲嘉宾：
刘小龙，中国科学院分子细胞科学卓越创新中心研究员，博士生导师。先后入选中国科学院“百人计划”国外引进杰出人才、国家“杰出青年科学基金项目”获得者和国家“万人计划”科技创新领军人才。近年来，系统研究了免疫细胞的分化成熟及功能作用机制，在Nat Immunol, Nat Commun和PNAS等学术期刊上发表50余篇研究论文。获明治乳业生命科学奖、第十一届中国青年科技奖和A-IMBN Research Young Investigators Award；被评为中国科学院优秀研究生指导教师和全国优秀博士学位论文指导教师；担任Cell Res和J Biol Chem等学术期刊的编委，任中国生物化学与分子生物学会秘书长。