TFAM deficiency in dendritic cells leads to mitochondrial dysfunction and enhanced antitumor immunity through cGAS-STING pathway

To investigate the role of TFAM knockout in the regulation of dendritic cell function, we cultured bone marrow-derived dendritic cells from wild type or Tfamflox/flox Cre-lyz2 mice, which were stimulated by tumor supernatant from LLC and harvested for RNA-seq analysis. Overall design: Comparative gene expression profiling analysis of RNA-seq data from wildtype or Tfamflox/flox Cre-lyz2 BMDCs treated with or without LLC tumor supernatant (TS) were carried out.