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IBD are chronic inflammatory disorders of the GI tract of unknown aetiology. Crohn's disease (CD) and UC may present with a variable clinical phenotype, and they run a highly variable disease course with a considerable proportion of patients with CD eventually developing penetrating or stricturing complications.1 The key mechanism underlying the pathogenesis of these diseases is assumed to be a dysregulated immune response to commensal flora in a genetically susceptible host.2 Thus, host genetics, the intestinal microbiota (commensal flora and dysbiosis) and external environmental factors are all thought to play an important role in the pathogenesis and in determining subsequent disease behaviour and outcomes. Genetic and recently microbiota research became a success story leading to a revolution in our understanding of the pathogenesis of IBDs and gave insight into the biology leading to new targeted treatment options. It all began with the identification of NOD2/CARD15 and unravelling the importance of innate immunity and defective bacterial sensing in 2001. Since then we have witnessed a rapid acceleration of gene discovery catalysed by the advent of genome-wide association studies, thanks to large collaborations of national and international groups.3 As of today, more than 160 IBD loci have been identified and these risk loci highlight several key pathways including innate immunity, adaptive immune responses, maintenance of intestinal barrier function, pathogen sensing, endoplasmic reticulum stress and response to oxidative stress.4 Of note, some important differences were noted between Europe and Asia (e.g. NOD2 or TNFSF15). In addition, most …
Contributors Both authors have contributed equally to the designing and writing of this commentary.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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