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A schematic diagram of immunological basis of cellular populations and mediator changes in IBD. Bacterial dysbiosis may result in overexpression of inflammatory cytokines (IL-1β, IL-6, and IFN-γ) by dendric cells and macrophages ultimately causing increased permeability of the gut epithelial cells. While Treg-cells secrete anti-inflammatory cytokine IL-10 and fibroblasts releases collagen and TGF-β for gut tissue repair.
