This study involves delineating how the strongest genetic risk factor for Crohn’s disease affects specific immune responses. We have found that this factor, NOD2, normally influences the nature of T cell responses when it detects microbes. We have mapped the molecules involved in this sensing process and wish to examine if Crohn’s patients with genetic risk factors in NOD2 show defective T cell responses as a result. Defining such pathways generates novel platforms to repair any defects identified therapeutically.
