Role of ATG16L, NOD2 and IL23R in Crohn's disease pathogenesis

• Published in: World journal of gastroenterology : WJG 2012-02, Vol.18 (5), p.412-424
• Main Authors: Naser, Saleh A, Arce, Melissa, Khaja, Anam, Fernandez, Marlene, Naser, Najih, Elwasila, Sammer, Thanigachalam, Saisathya
• Format: Article
• Language: English
• Subjects: Autophagy-Related Proteins; Carrier Proteins - genetics; Crohn Disease - epidemiology; Crohn Disease - genetics; Crohn Disease - physiopathology; CTLA-4 Antigen - genetics; Genetic Predisposition to Disease; Humans; Nod2 Signaling Adaptor Protein - genetics; Polymorphism, Genetic; Receptors, Interleukin - genetics; Review
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v18.i5.412

Inflammatory bowel disease is a group of diseases that includes Crohn's disease (CD) and ulcerative colitis. CD is characterized as a chronic inflammatory disease of the gastrointestinal tract, ranging from the mouth to the anus. Although there are gross pathological and histological similarities between CD and Johne's disease of cattle, the cause of CD remains controversial. It is vital to understand fully the cause of this disease because it affects approximately 500,000 people in North America and Europe. It ranges from 27 to 48 cases per 100,000 people. There are many theories on the cause of CD ranging from possible association with environmental factors including microorganisms to imbalance in the intestinal normal flora of the patients. Regardless of the environmental trigger, there is strong evidence that a genetic disposition is a major key in acquiring CD. Many studies have proven the link between mutations in the ATG16L, NOD2/CARD15, IBD5, CTLA4, TNFSF15 and IL23R genes, and CD. The purpose of this review is to examine all genetic aspects and theories of CD, including up to date multiple population studies performed worldwide.