ABSTRACT
Crohn’s disease (CD) and ulcerative colitis (UC) are two major forms of idiopathic inflammatory bowel disease (IBD) affecting 1.4 million individuals in the United States and 2.2 million in Europe (Economou and Pappas 2008). IBD, especially CD, are now widely accepted as complex multifactor diseases that occur in individuals with genetic predisposition in whom environmental and microbial triggers cause a deleterious chronic immune response (Stappenbeck et al. 2011; Kaser et al. 2010; Xavier and Podolsky 2007; Chassaing and Darfeuille-Michaud 2011). Over the last decade, genetic studies have emphasized the role of host susceptibility in IBD onset with the identifi cation of about one hundred risk loci. It is striking that most susceptibility genes identifi ed belong to a restricted number of pathways involved in intestinal barrier function, autophagy, microbial
Clermont Université, Université d’Auvergne, Clermont-Ferrand, France; Inserm U1071, Clermont-Ferrand, France; INRA, USC2018, Clermont-Ferrand, France; and Centre Hospitalier Universitaire, Clermont-Ferrand, France.
