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Inflammatory bowel disease (IBD) is a chronic condition that causes inflammation and swelling in the digestive tract. Although two types of IBD exist, Crohn's disease (CD) and Ulcerative Colitis, this review will focus mainly on CD. The common pathology in IBD is the induction of interleukins and an abnormal Paneth cell phenotype. CD is caused by environmental and multigenic factors, including mutations in NOD2 and RUNX-3. NOD2 promotes the induction of specific antimicrobial peptides that strengthen the immune system's response against antigens. Mutations in NOD2 cause an overexpression of NF-kB activity and IL-1-ß processing, which increases susceptibility to CD. Deletion of RUNX-3 in mice induces colitis and causes an increase in certain interleukins. Moreover, IL-23R induces a pro-inflammatory response while IL-11R promotes an anti-inflammatory response. Defective autophagy has been linked to abnormal Paneth cells and an endotoxin-induced inflammatory response in mice. The most promising CD treatments involve procedures that reduce inflammation by decreasing interleukin levels. Specifically, injection of anti-interleukin 12 antibodies, increasing the production of glucocorticoids through LRH-1, and the addition of polysaccharide A (PSA) can all serve as possible treatments for CD by down-regulating the overactive immune system. Identifying more genes that increase susceptibility to CD can lead to novel treatments in the future.


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