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Current concepts of celiac disease pathogenesis.

D Schuppan1

  • 1First Department of Medicine, University of Erlangen-Nuernberg, Erlangen, Germany. detlef.schuppan@med1.imed.uni-erlangen.de

Gastroenterology
|July 13, 2000
PubMed
Summary

Celiac disease results from genetic and environmental factors, involving gluten peptides and specific immune cells. Early screening for tissue transglutaminase antibodies is recommended due to links with other autoimmune conditions.

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[Comment].

Zeitschrift fur Gastroenterologie·2015

Area of Science:

  • Immunology
  • Gastroenterology
  • Genetics

Background:

  • Celiac disease pathogenesis involves a complex interplay of genetic and environmental factors.
  • Clinical manifestations vary widely, from asymptomatic cases to severe malabsorption.
  • Gluten peptides are key triggers in genetically susceptible individuals.

Purpose of the Study:

  • To elucidate the intricate mechanisms underlying celiac disease pathogenesis.
  • To highlight the role of specific immune responses in disease development.
  • To discuss potential future therapeutic strategies and screening recommendations.

Main Methods:

  • Analysis of immune cell interactions and antigen presentation in celiac disease.
  • Identification of autoantigens like tissue transglutaminase.
  • Investigation of the impact of inflammation on mucosal tissues.

Main Results:

  • Gluten peptides are presented by HLA-DQ2/DQ8-positive cells, driving immune responses in the lamina propria.
  • Tissue transglutaminase acts as a specific autoantigen, potentiating antigen presentation.
  • T-cell activation and mucosal transformation occur due to activated fibroblasts.

Conclusions:

  • Celiac disease is an immune-mediated disorder triggered by gluten in genetically predisposed individuals.
  • Untreated celiac disease increases the risk of other autoimmune diseases.
  • Population screening for tissue transglutaminase antibodies is warranted.

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