Abstract
Crohn's disease is one of two idiopathic inflammatory bowel diseases that affect approximately 1 million people in North America. Despite important advances in diagnosis and treatment in recent years, the underlying cause of the disease remains unclear. As a result, the available therapies are not curative and may pose a substantial risk of side effects. A current theory regarding the pathogenesis of Crohn's disease suggests that there is an overly aggressive immune response against commensal bacteria in a genetically predisposed person. In this context, the activation of lymphocytes and the overexpression of inflammatory cytokines represent a common effector mechanism leading . . .