Inflammatory bowel disease: Pathogenesis

Inflammatory bowel disease: Pathogenesis

January 7, 2014 | Yi-Zhen Zhang, Yong-Yu Li
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation. The pathogenesis of IBD involves a complex interaction between genetic, environmental, microbial, and immune factors. Recent advances in genetics have identified 163 susceptibility gene loci for IBD, with overlapping genes implicated in both childhood-onset and adult-onset IBD. However, genetic factors account for only a portion of the overall disease variance, suggesting that microbial and environmental factors may interact with genetic elements. Adaptive immune responses have traditionally been considered the primary driver of IBD, but recent studies have highlighted the importance of the innate immune response in inducing gut inflammation. Innate immune responses, including epithelial barrier integrity, innate microbial sensing, autophagy, and the unfolded protein response, are crucial in maintaining cellular homeostasis and defense against intracellular microorganisms. Adaptive immune responses, particularly Th17 cells, also play a significant role in the pathogenesis of IBD. The review provides an update on the major advances in these areas and highlights future research directions to better understand the complex interplay between genetic, environmental, microbial, and immune factors in IBD.Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation. The pathogenesis of IBD involves a complex interaction between genetic, environmental, microbial, and immune factors. Recent advances in genetics have identified 163 susceptibility gene loci for IBD, with overlapping genes implicated in both childhood-onset and adult-onset IBD. However, genetic factors account for only a portion of the overall disease variance, suggesting that microbial and environmental factors may interact with genetic elements. Adaptive immune responses have traditionally been considered the primary driver of IBD, but recent studies have highlighted the importance of the innate immune response in inducing gut inflammation. Innate immune responses, including epithelial barrier integrity, innate microbial sensing, autophagy, and the unfolded protein response, are crucial in maintaining cellular homeostasis and defense against intracellular microorganisms. Adaptive immune responses, particularly Th17 cells, also play a significant role in the pathogenesis of IBD. The review provides an update on the major advances in these areas and highlights future research directions to better understand the complex interplay between genetic, environmental, microbial, and immune factors in IBD.
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