In the healthy gastrointestinal tract, homeostasis is an active process that requires a careful balance of host responses to the enteric luminal contents. Intestinal macrophages and dendritic cells (DCs) comprise a unique group of tissue immune cells that are ideally situated at the interface of the host and the enteric luminal environment to appropriately respond to microbes and ingested stimuli. However, intrinsic defects in macrophage and DC function contribute to the pathogenesis of inflammatory bowel diseases, as highlighted by recent genome-wide association studies. Gastrointestinal macrophages and DCs participate in inflammatory bowel disease development through inappropriate responses to enteric microbial stimuli, inefficient clearance of microbes from host tissues, and impaired transition from appropriate proinflammatory responses to anti-inflammatory responses that promote resolution. By understanding how intestinal macrophages and DCs initiate chronic inflammation, new pathogenesis-based therapeutic strategies to treat human inflammatory bowel diseases will be elucidated.
Article first published online 23 August 2013
*Department of Microbiology and Immunology, University of North Carolina School of Medicine, Chapel Hill, North Carolina; and
†Center for Gastrointestinal Biology and Diseases, Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Reprints: Scott E. Plevy, MD, Center for Gastrointestinal Biology and Diseases, Department of Medicine, University of North Carolina School of Medicine, 103 Mason Farm Road, Campus Box 7032, 7341C MBRB, Chapel Hill, NC 27599-7032 (e-mail: email@example.com).
Funding Support: NIH NIDDK F30 DK089692 (ECS), NIH NIDDK R01 DK054452 (SEP).
The authors have no conflicts of interest to disclose.
Received July 09, 2013
Accepted July 24, 2013