Vitamin D, vitamin D receptor gene polymorphisms, and inflammatory bowel disease outcomes: From molecular mechanisms to clinical application

Figure 2 Schematic representation of the interplay between vitamin D metabolism, immune regulation, and intestinal homeostasis. Vitamin D modulates T cell differentiation (regulatory T cell, T helper 1, and T helper 17), regulates calcium metabolism, and influences gut microbiota composition. Vitamin D receptor (VDR)-mediated signaling controls the expression of tight junction proteins, such as claudin-2, and stimulates mucus production by goblet cells, thereby promoting intestinal barrier integrity. Genetic polymorphisms in the VDR (SNPs) may disrupt these pathways, increasing intestinal permeability and favoring inflammatory responses. This figure was created by the authors using BioRender (Supplementary material). Tregs: Regulatory T cells; Th1: T helper 1; Th17: T helper 17; CLDN2: Claudin-2; VDR: Vitamin D receptor; SNPs: Single-nucleotide polymorphisms; NF-кB: Nuclear factor kappa B.