Cells in the human body continuously undergo spontaneous mutations, some of them targeting proto-oncogenes or tumor suppressor genes. These are counteracted by the immune system that is nowadays widely accepted to be able to identify and subsequently eliminate cancerous self. This process is referred to as tumor immune surveillance. We are investigating surveillance of hematopoietic but also solid tumors in mouse models. Our focus lies on the Jak/Stat pathway, in particular interferon signaling, and its role in tumor immune surveillance.
The image above shows an effect of impaired tumor surveillance upon ablation of interferon signaling. Two weeks after intravenous injection of B16F10 melanoma cells the lung/body weight ratio was higher in mice with impaired type I interferon (IFN) signaling when compared with wildtype (WT) mice due to increased numbers of tumor nodules in the lung.
The image above summarises cellular and soluble players (such as type I interferons) in tumor immune surveillance.