Article citations

    A. Tripathi, K. M. Lammers, S. Goldblum et al., “Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 39, pp. 16799–16804, 2009.

has been cited by the following article:

  • TITLE: Novel Therapeutic/Integrative Approaches for Celiac Disease and Dermatitis Herpetiformis
  • AUTHORS: Alessio Fasano
  • JOURNAL NAME: Journal of Immunology Research DOI: 10.1155/2012/959061 Sep 16, 2014
  • ABSTRACT: Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. Gluten is a protein component in wheat and other cereals like rye and barley. At present, the only available treatment is a strict gluten-free diet. Recent advances have increased our understanding of the molecular basis for this disorder. Last decade has seen new scientific developments in this disease and led to the formulation of new concepts of pathophysiology that offer possible targets for new treatments or interventions integrative to the gluten-free diet. 1. Introduction Celiac disease (CD) is an immune-mediated chronic enteropathy with a wide range of presenting manifestations of variable severity. It is triggered by the ingestion of gliadin fraction of wheat gluten and similar alcohol-soluble proteins (prolamins) of barley and rye in genetically susceptible subjects with subsequent immune reaction leading to small bowel inflammation and normalization of the villous architecture in response to a gluten-free diet (GFD). CD not only affects the gut, but it is a systemic disease that may cause injury to the skin (dermatitis herpetiformis, the topic of this special issue), liver, joints, brain, heart, and other organs. It is a complex genetic disorder, and human leukocyte antigen (HLA) status appears to be the strongest genetic determinant of risk for celiac autoimmunity. There is a propensity for individuals with CD to carry specific HLA class II alleles, which has been estimated to account for up to 40% of the genetic load [1]. In affected individuals, 95% have either DQ2 (HLA-DQA1*05-DQB1*02) or DQ8 (HLADQA1*03-DQB1*0302), in comparison with the general population in which 39.5% have either DQ2 or DQ8 [2]. It is the interplay between genes (both HLA and non-HLA associated) and environment (i.e., gluten) that leads to the intestinal damage typical of the disease [3]. Under physiological circumstances, this interplay is prevented by competent intercellular tight junctions (TJs), structures that limit the passage of macromolecules (including gluten) across the intestinal epithelial barrier. Recent evidence suggests that the gluten-induced upregulation of zonulin, a recently described intestinal peptide involved in TJ regulation, is responsible, at least in part, for the aberrant increase in gut permeability characteristic of the early phase of CD [4] and the subsequent abnormal passage of gluten into the lamina propria. Here, the protein is deamidated by tissue transglutaminase and is then recognized by HLA-DQ2/DQ8