Inflammatory Bowel Disease: Pathobiology

Abstract

The current theory on the etiology of inflammatory bowel disease involves the interaction between a triggering environmental factor, possibly in the microbiome, and an individual susceptible to the disease due to genetic defects in immune function and regulation. To date over 300 genes and over 20 bacteria and viruses have been associated with the disease. No single factor is causative of the disease. Instead, an interplay of these factors leads to an inappropriate immune response resulting in the clinical characteristics or phenotype of the disease. Defects in the main innate immune functions of epithelial barrier function, pathogen recognition, and autophagy as well as adaptive immune dysfunction, particularly in T cell activation, differentiation, and function, have all been implicated in the disease.