How infection can incite sensitivity to food

@article{Verdu2017HowIC,
  title={How infection can incite sensitivity to food},
  author={Elena F. Verdu and Alberto Caminero},
  journal={Science},
  year={2017},
  volume={356},
  pages={29 - 30}
}
Microbes can trigger chronic immune disorders to dietary antigens, such as in celiac disease Immune tolerance to dietary antigens is key to preventing undesirable responses to innocuous antigens ingested with food. On page 44 of this issue, Bouziat et al. (1) report how viral infection may break oral tolerance to dietary proteins. The findings provide an explanation for the known epidemiological association between viral infections and the onset of food sensitivities, such as celiac disease… Expand
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References

SHOWING 1-10 OF 14 REFERENCES
Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease
TLDR
A viral infection model that makes use of two reovirus strains that infect the intestine but differ in their immunopathological outcomes discovered that it can nonetheless disrupt intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion and promoting TH1 immunity to dietary antigen. Expand
Triggers and drivers of autoimmunity: lessons from coeliac disease
TLDR
It is proposed that other exogenous factors might be identified as drivers of autoimmune processes, in particular when evidence for T cells with specificity for self antigens driving the disease is lacking. Expand
Novel players in coeliac disease pathogenesis: role of the gut microbiota
TLDR
The importance of utilizing animal models and long-term clinical studies to gain insight into the mechanisms through which host–microbial interactions can influence host responses to gluten and how the interplay between host genetics, environmental factors and the intestinal microbiota might contribute to its pathogenesis is highlighted. Expand
Duodenal Bacteria From Patients With Celiac Disease and Healthy Subjects Distinctly Affect Gluten Breakdown and Immunogenicity.
TLDR
This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie the reported association of dysbiosis and CD. Expand
Identification of tissue transglutaminase as the autoantigen of celiac disease
TLDR
Tissue transglutaminase is identified as the unknown endomysial autoantigen of celiac disease, and gliadin is a preferred substrate for this enzyme, giving rise to novel antigenic epitopes. Expand
Rotavirus Infection Frequency and Risk of Celiac Disease Autoimmunity in Early Childhood: A Longitudinal Study
TLDR
This prospective study provides the first indication that a high frequency of rotavirus infections may increase the risk of celiac disease autoimmunity in childhood in genetically predisposed individuals. Expand
Enhanced Expression of Interferon Regulatory Factor-1 in the Mucosa of Children with Celiac Disease
TLDR
Analysis of the expression of interferon (IFN) regulatory factor (IRF)-1 in Celiac disease suggests that IFN-γ/IRF-1 signaling pathway can play a key role in maintaining and expanding the local Th1 inflammatory response in this disease. Expand
The Oslo definitions for coeliac disease and related terms
TLDR
A multidisciplinary task force of 16 physicians from seven countries used the electronic database PubMed to review the literature for CD-related terms and suggested a definition for each term, followed by feedback through a web survey on definitions and discussions during a meeting in Oslo. Expand
Evidence for the role of interferon-alfa production by dendritic cells in the Th1 response in celiac disease.
TLDR
These data suggest that IFN-alfa-producing DCs contribute to the Th1 response in celiac disease. Expand
IL-15 functions as a danger signal to regulate tissue-resident T cells and tissue destruction
TLDR
It is proposed that expression of IL-15 in tissues promotes T helper 1 cell-mediated immunity and provides co-stimulatory signals to effector cytotoxic T cells to exert their effector functions and drive tissue destruction. Expand
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