Inflammatory bowel disease: genetic and epidemiologic considerations

World J Gastroenterol. 2008 Jan 21;14(3):338-47. doi: 10.3748/wjg.14.338.

Abstract

Genome-wide association studies have firmly established that many genomic loci contribute to inflammatory bowel disease, especially in Crohn's disease. These studies have newly-established the importance of the interleukin 23 and autophagy pathways in disease pathogenesis. Future challenges include: (1) the establishment of precisely causal alleles, (2) definition of altered functional outcomes of associated and causal alleles and (3) integration of genetic findings with environmental factors.

Publication types

  • Review

MeSH terms

  • Autophagy-Related Proteins
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Chromosomes, Human, Pair 5
  • Genetic Predisposition to Disease
  • Genome, Human
  • HLA Antigens / genetics
  • HLA Antigens / metabolism
  • Humans
  • Inflammatory Bowel Diseases* / epidemiology
  • Inflammatory Bowel Diseases* / genetics
  • Nod2 Signaling Adaptor Protein / genetics
  • Nod2 Signaling Adaptor Protein / metabolism
  • Polymorphism, Single Nucleotide
  • Receptors, Interleukin / genetics
  • Receptors, Interleukin / metabolism
  • Risk Factors
  • Tumor Necrosis Factor Ligand Superfamily Member 15 / genetics
  • Tumor Necrosis Factor Ligand Superfamily Member 15 / metabolism

Substances

  • ATG16L1 protein, human
  • Autophagy-Related Proteins
  • Carrier Proteins
  • HLA Antigens
  • IL23R protein, human
  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein
  • Receptors, Interleukin
  • TNFSF15 protein, human
  • Tumor Necrosis Factor Ligand Superfamily Member 15