Journal
IMMUNITY
Volume 36, Issue 6, Pages 907-919Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2012.06.006
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Funding
- INSERM
- Ligue Contre le Cancer
- Fondation Pour la Recherche Medicale
- Agence Nationale pour la Recherche
- Association pour la Recherche contre le Cancer
- Association francaise des Patients Intolerants au Gluten
- Fondation Princesse Grace
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Celiac disease (CD) is a chronic enteropathy induced by dietary gluten in genetically predisposed people. The keystone of CD pathogenesis is an adaptive immune response orchestrated by the interplay between gluten and MHC class II HLA-DQ2 and DQ8 molecules. Yet, other factors that impair immunoregulatory mechanisms and/or activate the large population of intestinal intraepithelial lymphocytes (IEL) are indispensable for driving tissue damage. Herein, we summarize our current understanding of the mechanisms and consequences of the undesirable immune response initiated by gluten peptides. We show that CD is a model disease to decipher the role of MHC class II molecules in human immunopathology, to analyze the mechanisms that link tolerance to food proteins and autoimmunity, and to investigate how chronic activation of IEL can lead to T cell lymphomagenesis.
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