Our research program seeks to dissect the complex dynamics of host-environment interactions required to sustain intestinal homeostasis and how breakdown in these interactions may lead to inflammatory bowel diseases (IBD). Although genome wide association studies (GWAS) have been instrumental in associating genetic variants/polymorphisms with IBD, assigning causality to these variants in IBD pathogenesis has proven to be difficult. In particular we are trying to understand how deregulation of intestinal immune homeostasis might lead to IBD and trying to discover the function of IBD-risk genes identified by Genome Wide Association Studies (GWAS). To discover the function of IBD-risk genes, we focus in biological processes that are involved at the initiation (priming of adaptive immune responses), progression (chronic inflammation) or resolution (tissue repair) of IBD. To translate genetic mutations to function, we have developed an innovative pipeline that integrate bioinformatics and animal models, including zebrafish and mouse, to ultimately validate candidates mutations in human tissues by using organoids.