Abstract
The primary pathogenic trigger in coeliac disease (CD) is still unknown. We present the hypothesis that in CD the enterocytes could metabolize gliadin through an immunogenic pathway instead of a tolerogenic one. The result of this abnormal presentation of gliadin to the immune system would be the activation of lamina propria T cells, followed by the onset of enteropathy.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Antigen-Presenting Cells / immunology*
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Antigens, CD / immunology
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Celiac Disease / immunology*
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Genes, MHC Class I / immunology
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Gliadin / immunology*
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Gliadin / metabolism
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Humans
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Immune System / immunology
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T-Lymphocytes / immunology*
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Transglutaminases / immunology
Substances
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Antigens, CD
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Gliadin
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Transglutaminases