Journal
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
Volume 5, Issue -, Pages 119-144Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathol.4.110807.092135
Keywords
tight junction; claudin; occludin; myosin light chain kinase; tumor necrosis factor; inflammatory bowel disease
Categories
Funding
- NCI NIH HHS [P30CA14599] Funding Source: Medline
- NHLBI NIH HHS [T32HL007605, T32HL007237] Funding Source: Medline
- NIDDK NIH HHS [R01DK61931, R01DK68271, P01DK067887] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA014599] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007237, T32HL007605] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK067887, R01DK061931, R01DK068271] Funding Source: NIH RePORTER
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Epithelia form barriers that are essential to life. This is particularly true in the intestine, where the epithelial barrier supports nutrient and water transport while preventing microbial contamination of the interstitial tissues. Along with plasma membranes, the intercellular tight junction is the primary cellular determinant of epithelial barrier function. Disruption of tight junction structure, as a result of specific protein mutations or aberrant regulatory signals, can be both a cause and an effect of disease. Recent advances have provided new insights into the extracellular signals and intracellular mediator of tight junction regulation in disease states as well as into the interactions of intestinal barrier functions with mucosal immune cells and luminal microbiota. In this review, we discuss the critical roles of the tight junction in health and explore the contributions of barrier dysfunction to disease pathogenesis.
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