| [ Summary ] |
The pathophysiology of inflammatory bowel disease(IBD) is still unknown, but recent studies have suggested that immune dysregulation caused by environmental factors, gut microbiota, and genetic predisposition plays an essential role in IBD development. Anti-tumor necrosis factor-alpha(TNF-α) has been shown to induce apoptosis of T cells and macrophages as well as the neutralization of the cytokine. Anti-IL-12/23p40 antibody inhibits both IL-12 and IL-23, which are produced by macrophages and dendritic cells and are thought to trigger subsequent acquired immune dysfunction. An integrin inhibitor suppresses the α4β7-dependent recruitment of lymphocytes into the gut, and Janus kinase inhibitors suppress the downstream inflammatory response of various cytokine receptors. |