Aiping M Zhao

Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.

Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms.

Jeroen Visser; Jan Rozing; Anna Sapone; Karen Lammers; Alessio Fasano (Profiled Authors: Alessio Fasano; Karen Lammers)

Department of Cell Biology, Section Immunology and Histology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Annals of the New York Academy of Sciences 2009;1165():195-205.

Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on celiac disease (CD), an autoimmune enteropathy, and type 1 diabetes (T1D), a hyperglycosaemia caused by a destructive autoimmune process targeting the insulin-producing pancreatic islet cells. Even if environmental factors and genetic susceptibility are clearly involved in the pathogenesis of autoimmunity, for most autoimmune disorders there is no or little knowledge about the causing agent or genetic makeup underlying the disease. In this respect, CD represents a unique autoimmune disorder because a close genetic association with HLA-DQ2 or HLA-DQ8 haplotypes and, more importantly, the environmental trigger (the gliadin fraction of gluten-containing grains wheat, barley, and rye) are known. Conversely, the trigger for autoimmune destruction of pancreatic ss cells in T1D is unclear. Interestingly, recent data suggest that gliadin is also involved in the pathogenesis of T1D. There is growing evidence that increased intestinal permeability plays a pathogenic role in various autoimmune diseases including CD and T1D. Therefore, we hypothesize that besides genetic and environmental factors, loss of intestinal barrier function is necessary to develop autoimmunity. In this review, each of these components will be briefly reviewed.

2 Originating Grant

• 1.

  Fasano, Alessio

  Timing of Gluten Intake In Infant Nutrition and Risk of Celiac Disease Autoimmuni

  15 April 2008 - 31 March 2010

  NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES

• 2.

  FASANO, ALESSIO

  Zot, Zonulin, and Pathophysiology of Intestinal Tight Junctions

  1 May 1996 - 31 July 2016

  NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES

Scientific Context

This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.