Recent advances in IBD pathogenesis: genetics and immunobiology.
The inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, are chronic inflammatory disorders caused by dysregulated immune responses in genetically predisposed individuals. Although the precise etiology of IBD remains unclear, accumulating data, including genome-wide association studies, have advanced our understanding of its immunopathogenesis. This review highlights the role in gut homeostasis and IBD pathogenesis of autophagy, the interleukin (IL)-23/IL-17 axis, and a novel member of the tumor necrosis factor family, TL1A. It focuses on advances in our understanding of IBD from the past year, including advances in genetics and immunobiology.
Shih
David Q
DQ
Cedars-Sinai Inflammatory Bowel Disease Center, 8700 Beverly Boulevard, Suite D4059, Los Angeles, CA 90048, USA. david10021@gmail.com
Targan
Stephan R
SR
McGovern
Dermot
D
D020022:Genetic Predisposition to Disease; D006801:Humans; D007107:Immune System / Q000503:physiopathology*; D015212:Inflammatory Bowel Diseases / Q000235:genetics* / Q000276:immunology*; D020381:Interleukin-17 / Q000378:metabolism; D053759:Interleukin-23 / Q000378:metabolism; D011110:Polymorphism, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D020381:Interleukin-17; D053759:Interleukin-23; D014409:Tumor Necrosis Factor-alpha