Figure 2.

Pathophysiology of inflammatory bowel disease. Multiple factors contribute to IBD. Changes in the microbiota accompanied by thinning of the mucus layer induces a barrier breach that results in defects in the epithelium. Crossing of the barrier by microbiota components induces DC and macrophage activation, which induces infiltration of the intestinal tissue by inflammatory CD4 T cells. IBD patients have an increased content of proinflammatory Th1 and Th17 cells. This infiltration is accompanied by an increase in Th2 cell numbers and insufficient numbers of immune suppressing cells, such as Tregs. Inflammatory T cells guide the function of cells with an innate immune role, such as epithelial cells, fibroblasts and phagocytes, thus stimulating a constant hyperresponsiveness to microbial antigens and causing tissue injury and chronic intestinal inflammation.