IL-23 drives innate and T cell-mediated intestinal inflammation. Inflammatory bowel disease (IBD) involves aberrant activation of innate and adaptive immune responses. This study shows that IL-23, but not IL-12, is essential for chronic intestinal inflammation. Depletion of IL-23 reduced proinflammatory responses in the intestine but had little impact on systemic T cell responses. IL-23 is a key driver of innate immune pathology in the intestine and represents an attractive therapeutic target for IBD. IL-23 is primarily secreted by activated dendritic cells, monocytes, and macrophages and supports the development of Th17 cells, which produce IL-17 and contribute to autoimmune tissue inflammation. IL-23 also affects innate immune cells, inducing the production of inflammatory cytokines. The study used two models of IBD: one involving innate immune activation by Helicobacter hepaticus and another involving T cell transfer. Results showed that IL-23 is essential for both innate and T cell-mediated intestinal inflammation. Anti-IL-23 treatment significantly reduced inflammation in both models. IL-23 is not required for systemic inflammatory responses but is essential for local intestinal inflammation. The study highlights the role of IL-23 in driving proinflammatory cytokine cascades and suggests that targeting IL-23 could be an effective therapeutic approach for IBD. The findings also indicate that IL-23 may be involved in the pathogenesis of other inflammatory diseases. The study provides new insights into the mechanisms of IBD and supports the development of targeted therapies for this condition.IL-23 drives innate and T cell-mediated intestinal inflammation. Inflammatory bowel disease (IBD) involves aberrant activation of innate and adaptive immune responses. This study shows that IL-23, but not IL-12, is essential for chronic intestinal inflammation. Depletion of IL-23 reduced proinflammatory responses in the intestine but had little impact on systemic T cell responses. IL-23 is a key driver of innate immune pathology in the intestine and represents an attractive therapeutic target for IBD. IL-23 is primarily secreted by activated dendritic cells, monocytes, and macrophages and supports the development of Th17 cells, which produce IL-17 and contribute to autoimmune tissue inflammation. IL-23 also affects innate immune cells, inducing the production of inflammatory cytokines. The study used two models of IBD: one involving innate immune activation by Helicobacter hepaticus and another involving T cell transfer. Results showed that IL-23 is essential for both innate and T cell-mediated intestinal inflammation. Anti-IL-23 treatment significantly reduced inflammation in both models. IL-23 is not required for systemic inflammatory responses but is essential for local intestinal inflammation. The study highlights the role of IL-23 in driving proinflammatory cytokine cascades and suggests that targeting IL-23 could be an effective therapeutic approach for IBD. The findings also indicate that IL-23 may be involved in the pathogenesis of other inflammatory diseases. The study provides new insights into the mechanisms of IBD and supports the development of targeted therapies for this condition.