PRESENTATIONSInnate Immunity in Crohn's Disease: The Reverse Side of the MedalDessein, Rodrigue MD*; Chamaillard, Mathias PhD†; Danese, Silvio MD, PhD‡Author Information *INSERM, U801 †INSERM, U795, Université Lille 2, Lille, France ‡Division of Gastroenterology, Istituto Clinico Humanitas, IRCCS in Gastroenterology, Rozzano, Milan, Italy Competing Interests: The authors have declared that no competing interests exist. Authors contribution: Mathias Chamaillard, Rodrigue Dessein, and Silvio Danese wrote the manuscript. The costs of this review is supported by a grant from INSERM to MC and the Italian Ministry of Health (Ricerca Finalizzata 2006, n. 72) to SD. Reprints: Mathias Chamaillard, PhD, INSERM, U795, Université Lille 2, Lille, France (e-mail: firstname.lastname@example.org). Correspondence: Silvio Danese, MD, PhD, Division of Gastroenterology, Instituto Clinico Humanitas, IRCCS in Gastroenterology, Milan, Italy (e-mail: email@example.com). Received for publication December 18, 2007; accepted December 19, 2007 Journal of Clinical Gastroenterology: September 2008 - Volume 42 - Issue - p S144-S147 doi: 10.1097/MCG.0b013e3181662c90 Buy Metrics Abstract The etiology of Crohn's disease (CD) remains poorly understood. Both mice and human studies suspected a perverse link between the microbiota and the lining of the gut mucosa. There is now emerging evidence that suggests that such a pathologic condition might result from an overly aggressive immune response to microbial antigens in genetically predisposed individuals. However, the multiple pathophysiologic processing steps linking environmental exposure to the clinical expression of CD are, for the most part, unknown. Herein, we review evidences reflecting a general causing defect of the innate immune function of the intestinal mucosa of CD patients, which might lead to a sustained microbial-induced inflammatory response. Changing the paradigms of CD pathophysiology might lead to entirely new therapeutic approaches aiming to boost the innate immune response. © 2008 Lippincott Williams & Wilkins, Inc.