Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is characterized by chronic intestinal inflammation driven by dysregulated immune responses in gut microbiota. Interleukin (IL)-23, a member of IL-12 cytokine family, has emerged as a key immune mediator, being produced mainly by macrophages from the intestinal mucosa. In recent years, vitamin D has become a pivotal immunomodulatory factor in IBD, vitamin D deficiency being commonly associated with this pathology. The immune effects of vitamin D are mediated through vitamin D receptor (VDR), widely expressed in macrophages and other immune cells. VDR signaling regulates pro-inflammatory macrophage activity and limits M1 polarization, therefore reducing IL-23 production and limiting Th17 driven inflammatory response. This review summarizes current evidence on the role of macrophage-derived IL-23 in IBD pathogenesis and highlights the modulatory effects of vitamin D/VDR signaling. In addition, it addresses the therapeutic relevance of targeting the VDR–macrophage–IL-23 axis in IBD.