γδ T cells have previously been shown to play a protective role in various animal models of chronic inflammation (e.g., experimental autoimmune encephalomyelitis, collagen-induced arthritis, and non-obese diabetes). This immunoregulatory potential is exerted by synthesizing various anti-inflammatory cytokines and growth factors (e.g., transforming growth factor-β). As the normal balance between inflammatory and regulatory cytokines is perturbed in inflammatory bowel disease (IBD) a protective effect of γδ T cells seems likely. This notion is supported by our finding of increased mortality of rats with 2,4,6-trinitrobenzene sulfonic acid-induced colitis following γδ T cell depletion. In contrast, no effect was observed after depletion of γδ T cells in a Crohn's disease animal model with terminal ileitis (TNFΔARE mice). Therefore, future studies must further define where in the intestinal immune system γδ T cells exert their protective function and how this can be used in the treatment of IBD.
Research Areas and Centers
- Academic Focus: Center for Infection and Inflammation Research (ZIEL)