Abstract

The gastrointestinal (GI) tract is home to a large number and vast array of bacteria that play an important role in nutrition, immune system development and host defense. In inflammatory bowel disease (IBD) there is a breakdown in this mutualistic relationship resulting in aberrant inflammatory responses that can progress to colon cancer. Our studies in model systems have implicated innate lymphoid cells and the IL-23/IL-22 axis as key drivers of neoplasia and cancer in the intestine. In this presentation I will discuss new checkpoints that control bacteria driven innate inflammation in the intestine as well as the functional effects of IL-22 on intestinal epithelial cells and interactions between IL-22 signalling and oncogenic mutations. Further understanding of the interactions between host genetics, gut microbiota, and deranged inflammatory pathways may yield new preventative and therapeutic  approaches to colorectal cancer.