The study investigates the role of interleukin (IL)-23 in intestinal inflammation, focusing on two models of inflammatory bowel disease (IBD). The results show that IL-23, but not IL-12, is essential for both innate and adaptive immune-mediated intestinal inflammation. In the *Helicobacter hepaticus*-induced model, IL-23 depletion reduced proinflammatory cytokine production and attenuated intestinal pathology. In the T cell transfer model, IL-23 deficiency significantly reduced colitis severity, suggesting its role in T cell-mediated inflammation. Additionally, IL-23 was found to induce IL-17 production by non-T cells, contributing to innate intestinal pathology. These findings highlight IL-23 as a key driver of intestinal inflammation and suggest that targeting IL-23 could be an effective therapeutic approach for IBD.The study investigates the role of interleukin (IL)-23 in intestinal inflammation, focusing on two models of inflammatory bowel disease (IBD). The results show that IL-23, but not IL-12, is essential for both innate and adaptive immune-mediated intestinal inflammation. In the *Helicobacter hepaticus*-induced model, IL-23 depletion reduced proinflammatory cytokine production and attenuated intestinal pathology. In the T cell transfer model, IL-23 deficiency significantly reduced colitis severity, suggesting its role in T cell-mediated inflammation. Additionally, IL-23 was found to induce IL-17 production by non-T cells, contributing to innate intestinal pathology. These findings highlight IL-23 as a key driver of intestinal inflammation and suggest that targeting IL-23 could be an effective therapeutic approach for IBD.