Volume 73 Number 8 December 2006	back to contents

¹Director, Inflammatory Bowel Disease Center and Associate Professor of Medicine and ²Present-Levison Inflammatory Bowel Disease Fellow, Mount Sinai School of Medicine, New York, NY.

Address all correspondence to Maria T. Abreu, M.D., Director, Inflammatory Bowel Disease Center, Associate Professor of Medicine, Mount Sinai School of Medicine, 1 East 100th Street, Box 1069, New York, NY 10029; e-mail: maria.abreu@mssm.edu

Acknowledgement of grant support for Maria T. Abreu, M.D.: Grant Research Support—Centocor, Proctor and Gamble; Consultant—Abbott, Proctor and Gamble, Prometheus; Speaker’s Bureau—Proctor and Gamble, Salix, Centocor, Prometheus.

Presented at the Department of Medicine, Mount Sinai School of Medicine, New York, NY on April 5, 2005, and updated September 2006.

Abstract

The idiopathic inflammatory bowel diseases (IBDs), broadly classified as either Crohn's disease (CD) or ulcerative colitis (UC), are caused by a dysregulated mucosal immune response to a luminal antigen, possibly a bacterium, in a genetically predisposed host. A rapid expansion of knowledge in recent years has greatly increased our understanding of the pathophysiology of these disorders. For example, the relatively recent discovery of the NOD2 gene, a protein involved in bacterial sensing, has provided further evidence of the complex interplay between hosts and microbes in Crohn's disease. Significant recent advances have also occurred with the discovery of the role of Toll-like receptors and dendritic cells in the development of gut inflammation, and the role of proinflammatory cytokines in the development and potentiation of gut inflammation. This article presents an update on these key developments and emphasizes the translational aspects of research that are directly related to patient care.

Key Words

Inflammatory bowel disease, Crohn's disease, ulcerative colitis, innate immunity, adaptive immunity, biological therapies

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