Toll-like receptors and innate immunity in gut homeostasis... : Current Opinion in Hematology (original) (raw)

Myeloid biology

aDivision of Gastroenterology, Inflammatory Bowel Disease Center, USA

bDivision of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Immunobiology and Burns and Allen Research Institutes, Cedars-Sinai Medical Center and David Geffen School of Medicine, University of California, Los Angeles, California, USA

Correspondence to Moshe Arditi, MD, Professor of Pediatrics, UCLA School of Medicine, Director, Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room 4220, Los Angeles, CA 90048, USA Tel: +1 310 423 4064; Fax: +1 310 423 8284; e-mail: [email protected]

Supported by NIH grants HL-66436 and AI-058128 to M.A.

Abstract

Purpose of review

Immune responses to commensal bacteria and resulting chronic inflammation are hallmarks of inflammatory bowel disease. Considerable evidence has accumulated to suggest that innate immune defense mechanisms interact with pro-inflammatory pathways and exacerbate or perhaps even initiate development of inflammatory bowel disease.

Recent findings

Recent cellular and mouse studies now show Toll-like receptor responses in intestinal epithelial cells are polarized and their activation by commensal bacteria plays an essential role in maintaining colonic homeostasis and controlling tolerance in the gut. Recent data also implicate signaling by Toll-like receptors and the common adaptor molecule MyD88 in intestinal epithelial homeostasis as well as the pathogenesis of inflammatory bowel disease, establishing a key link between the innate and adaptive immune defenses.

Summary

We review recent progresses in the understanding of the role of Toll-like receptors and other pattern recognition receptors in the host defense against gastrointestinal pathogens and maintenance of immune tolerance to commensal bacteria, highlighting areas that should provide fertile ground for future studies aimed at a more comprehensive understanding of the interplay between innate and adaptive immune defense mechanisms and inflammatory bowel disease.