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Sci. STKE, 3 January 2006
Vol. 2006, Issue 316, p. pe1
[DOI: 10.1126/stke.3162006pe1]

PERSPECTIVES

The Significance of Interferon-{gamma}–Triggered Internalization of Tight-Junction Proteins in Inflammatory Bowel Disease

Hideki Chiba*, Takashi Kojima, Makoto Osanai, and Norimasa Sawada

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo 060–8556, Japan.

Summary: Disruption of the epithelial barrier function of tight junctions by the proinflammatory cytokine interferon (IFN)–{gamma} plays a fundamental role in the pathogenesis of inflammatory bowel disease and other gastrointestinal disorders, but its precise mechanism has not been established. This Perspective provides an overview of how IFN-{gamma} triggers barrier dysfunction and bacterial translocation in intestinal epithelial cells, and highlights the roles of internalization of tight-junction transmembrane proteins, as well as rearrangements of the cortical actin cytoskeleton, in intestinal inflammation.

*Corresponding author. E-mail, hidchiba{at}sapmed.ac.jp

Citation: H. Chiba, T. Kojima, M. Osanai, N. Sawada, The Significance of Interferon-{gamma}–Triggered Internalization of Tight-Junction Proteins in Inflammatory Bowel Disease. Sci. STKE 2006, pe1 (2006).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Mechanism of IL-1{beta}-Induced Increase in Intestinal Epithelial Tight Junction Permeability.
R. Al-Sadi, D. Ye, K. Dokladny, and T. Y. Ma (2008)
J. Immunol. 180, 5653-5661
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