ReviewJournal of clinical medicine2026
Vitamin D Receptor-Macrophage-IL-23 Axis in Inflammatory Bowel Disease: Pathogenic Mechanisms and Therapeutic Hope.
Review in Journal of clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
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.
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