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P31–43, an undigested gliadin peptide, mimics and enhances the innate immune response to viruses and interferes with endocytic trafficking: a role in celiac disease
- Source :
- Scientific Reports, Scientific Reports, Vol 8, Iss 1, Pp 1-12 (2018)
- Publication Year :
- 2018
- Publisher :
- Springer Science and Business Media LLC, 2018.
-
Abstract
- Celiac disease (CD) is an autoimmune disease characterized by inflammation of the intestinal mucosa due to an immune response to wheat gliadins. Some gliadin peptides are resistant to intestinal digestion (e.g., A-gliadin P31–43) and induce a stress/innate immune response, but the reason why they are dangerous in the intestines of patients with CD is unknown. In the present study, P31–43 activated IFN-α, a mediator of the innate immune response in CD, in the intestine of subjects with CD and an enterocyte cell line, CaCo-2. P31–43 cooperated with a viral ligand to activate the TLR7 pathway by interfering with endocytic trafficking. Based on these results, the vesicular pathway regulates the innate/inflammatory response to viral ligands and bioactive dietary peptides. Suggesting that together with viral infections, alimentary proteins able to mimic and potentiate the innate immune response to viruses, can trigger an autoimmune disease such as CD.
- Subjects :
- Male
Myxovirus Resistance Proteins
0301 basic medicine
Adolescent
lcsh:Medicine
Inflammation
Biology
Gliadin
Article
Diet, Gluten-Free
03 medical and health sciences
Immune system
Intestinal mucosa
Immunity
medicine
Humans
Intestinal Mucosa
lcsh:Science
Child
Autoimmune disease
Multidisciplinary
Innate immune system
Guanosine
lcsh:R
NF-kappa B
Interferon-alpha
TLR7
medicine.disease
Endocytosis
Immunity, Innate
Peptide Fragments
Celiac Disease
Enterocytes
030104 developmental biology
Toll-Like Receptor 7
Child, Preschool
Immunology
lcsh:Q
Female
Gluten free
Caco-2 Cells
medicine.symptom
Signal Transduction
Subjects
Details
- ISSN :
- 20452322
- Volume :
- 8
- Database :
- OpenAIRE
- Journal :
- Scientific Reports
- Accession number :
- edsair.doi.dedup.....b94a2810fde97fcf0af020824ece9c7b