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.
aMedStar Georgetown Transplant Institute, Georgetown University Hospital, Northwest, Washington, DC
bDepartment of Surgery, Walter Reed National Military Medical Center, Bethesda, Maryland
cDepartment of Gastroenterology, Hepatology and Nutrition, Children's National Medical Center, Northwest, Washington, DC, USA
Correspondence to Alexander Kroemer, MedStar Georgetown Transplant Institute, 2 PHC, Georgetown University Hospital, 3800 Reservoir Rd., Northwest, WA 20007, USA. Tel: +1 202 444 3700; fax: +1 877 680 8192; e-mail: firstname.lastname@example.org,email@example.com