Inflammatory bowel disease (IBD) is a chronic disease in the gastrointestinal tract (GIT). IBD include ulcerative colitis (UC), which generally affects only the large intestine mucosa and submucosa, and Crohn’s disease (CD), which may affect any part of the GIT by transmural inflammation. Both UC and CD are associated with an imbalance of the gut microbiota composition and injuries in the intestinal mucosa. The intestinal dysbiosis is related to a reduction in butyrate-producing species, impairing the anti-inflammatory response of the immune system, and is commonly associated with micronutrients deficiency, e.g. vitamin D hypovitaminosis. Vitamin D is involved in several critical functions, including immune cell differentiation, regulation of microbiota, gene transcription, and barrier integrity. Vitamin D supplementation in IBD patients showed promising results in reducing the disease activity and modulating gut microbiota. Vitamin D receptor (VDR) regulates the biological actions of the active vitamin D metabolite, 1α,25-dihydroxyvitamin D3. Evidence supports that the VDR signaling is involved in the genetic, environmental, immune, and microbial aspects of IBD. Low VDR expression and dysfunction of vitamin D/VDR signaling are reported in IBD patients. Vitamin D/VDR deficiency could be considered as a multifunctional susceptibility factor in IBD. Therefore, in this review, we will discuss the progress in clinical studies, mechanism studies on Vitamin D /VDR, and potential use of vitamin D supplementation as adjuvant therapy to restore gut microbiota balance, promote beneficial metabolites, and inhibit inflammation status in patients with IBD.