The parallel paradigm between intestinal transplant inflammation and inflammatory bowel disease.

Abstract

A significant shift in our understanding of the molecular and cellular basis for inflammatory bowel disease (IBD) mirrors research that has been ongoing in intestinal transplantation. The blurring of lines between these two disease states creates an avenue into potential therapeutic interventions which take advantage of these molecular similarities. Traditional knowledge of T-cell involvement in IBD has expanded to highlight the role of T helper 17 (Th17) cells as key effector cells. A similar role has been demonstrated in cellular rejection of intestinal allografts. Genetic polymorphism related to the propagation and function of Th17 cells has been found to confer significant risk of developing autoimmune conditions. Interleukin-23, a cytokine identified as crucial to the expansion of Th17 cells, has become a validated molecular target in psoriatic arthritis and IBD, and could become a target for intestinal transplant therapies. Intestinal transplant rejection and IBD share a similar phenotype, especially as it relates to key effector cells and gene polymorphisms. Improvements in our understanding of the immune-pathogenesis of IBD, as well as molecular targeting exploiting that knowledge, provide a potential route to improve outcomes for intestinal transplant patients.