Abstract
Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory condition of the intestines that is clinically heterogenous. The cause(s) of IBD are currently unknown but the mechanisms of injury are immunological. Increasingly there is an emphasis on the study of the complex interactions at the interface of self and non-self--the gastrointestinal epithelial surface--in relationship to the pathogenesis of disease. There is mounting evidence that a lack of tolerance to the normal commensal flora of the intestine may underlie the disease pathogenesis. Several genetic loci that are markers of disease susceptibility have been identified. These loci map to areas of the genome that are concerned with antigen presentation or cytokine secretion and suggest a genetic heterogeneity that underlies the clinical differences. Overall a picture is emerging of defects in epithelial barrier function and, or immunoregulation leading to immune responses that are triggered or exaggerated by the antigenic components of the normal flora.