Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), have a complex immunopathogenesis involving chronic, dysregulated inflammation of the gut in response to commensal microbes. Current therapies, such as Anti-TNF drugs, target this immune dysregulation, but many patients exhibit recurrent inflammation despite treatment (refractoriness). Research shows that IBD patient phagocytic immune cells have altered cytokine production and bacterial clearing defects.