Table of Contents
Journal of Allergy
Volume 2012 (2012), Article ID 596081, 11 pages
Review Article

Intestinal Epithelial Barrier Dysfunction in Food Hypersensitivity

Graduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, no. 1 Jen-Ai Road Section I, Taipei 100, Taiwan

Received 26 May 2011; Revised 6 July 2011; Accepted 8 July 2011

Academic Editor: Kirsi Laitinen

Copyright © 2012 Linda Chia-Hui Yu. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Intestinal epithelial barrier plays a critical role in the maintenance of gut homeostasis by limiting the penetration of luminal bacteria and dietary allergens, yet allowing antigen sampling for the generation of tolerance. Undigested proteins normally do not gain access to the lamina propria due to physical exclusion by tight junctions at the cell-cell contact sites and intracellular degradation by lysosomal enzymes in enterocytes. An intriguing question then arises: how do macromolecular food antigens cross the epithelial barrier? This review discusses the epithelial barrier dysfunction in sensitized intestine with special emphasis on the molecular mechanism of the enhanced transcytotic rates of allergens. The sensitization phase of allergy is characterized by antigen-induced cross-linking of IgE bound to high affinity FcεRI on mast cell surface, leading to anaphylactic responses. Recent studies have demonstrated that prior to mast cell activation, food allergens are transported in large quantity across the epithelium and are protected from lysosomal degradation by binding to cell surface IgE and low-affinity receptor CD23/FcεRII. Improved immunotherapies are currently under study including anti-IgE and anti-CD23 antibodies for the management of atopic disorders.