ArticlePloS one2013
Intestinal T-cell responses in celiac disease - impact of celiac disease associated bacteria.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Innate immune dysregulation in celiac disease and refractory celiac disease: mechanisms, management and emerging therapies.Frontiers in immunology · 2026Review
- Bacteria: Potential Make-or-Break Determinants of Celiac Disease.International journal of molecular sciences · 2024Review
- Celiac Disease: A Review from Genetic to Treatment.Iranian biomedical journal · 2024Review
- Celiac Disease Predisposition and Genital Tract Microbiota in Women Affected by Recurrent Pregnancy Loss.Nutrients · 2023Article
- The pathogenesis of cryptoglandular anal fistula: New insight into the immunological profile.Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland · 2022Article
- Article
- Gastrointestinal Tract Microbiome Effect and Role in Disease Development.Diseases (Basel, Switzerland) · 2022Review
- Gut microbiota in various childhood disorders: Implication and indications.World journal of gastroenterology · 2022Review
- A comprehensive map of microbial biomarkers along the gastrointestinal tract for celiac disease patients.Frontiers in microbiology · 2022Article
- Why are western diet and western lifestyle pro-inflammatory risk factors of celiac disease?Frontiers in nutrition · 2022Review
- Potential impact of celiac disease genetic risk factors on T cell receptor signaling in gluten-specific CD4+ T cells.Scientific reports · 2021Article
- Contribution of Infectious Agents to the Development of Celiac Disease.Microorganisms · 2021Review
- Intestinal Microbiota in Common Chronic Inflammatory Disorders Affecting Children.Frontiers in immunology · 2021Review
- Fecal microRNAs as Innovative Biomarkers of Intestinal Diseases and Effective Players in Host-Microbiome Interactions.Cancers · 2020Review
- Celiac Disease and Non-celiac Wheat Sensitivity: State of Art of Non-dietary Therapies.Frontiers in nutrition · 2020Review
- Celiac Disease and the Microbiome.Nutrients · 2019Review
- The Gut Microbiota in Celiac Disease and probiotics.Nutrients · 2019Review
- Effect of gluten diet on blood innate immune gene expressions and stool consistency in Spix's Saddleback Tamarin (Leontocebus fuscicollis) raised in captivity.Molecular biology reports · 2019Article
- Vibrio cholerae derived outer membrane vesicles modulate the inflammatory response of human intestinal epithelial cells by inducing microRNA-146a.Scientific reports · 2019Article
- IL-17 and limits of success.Cellular immunology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of active celiac disease (CD), an inflammatory small-bowel enteropathy caused by permanent intolerance to gluten, is cytokine production by intestinal T lymphocytes. Prerequisites for contracting CD are that the individual carries the MHC class II alleles HLA-DQ2 and/or HLA-DQ8 and is exposed to gluten in the diet. Dysbiosis in the resident microbiota has been suggested to be another risk factor for CD. In fact, rod shaped bacteria adhering to the small intestinal mucosa were frequently seen in patients with CD during the "Swedish CD epidemic" and bacterial candidates could later be isolated from patients born during the epidemic suggesting long-lasting changes in the gut microbiota. Interleukin-17A (IL-17A) plays a role in both inflammation and anti-bacterial responses. In active CD IL-17A was produced by both CD8(+) T cells (Tc17) and CD4(+) T cells (Th17), with intraepithelial Tc17 cells being the dominant producers. Gluten peptides as well as CD associated bacteria induced IL-17A responses in ex vivo challenged biopsies from patients with inactive CD. The IL-17A response was suppressed in patients born during the epidemic when a mixture of CD associated bacteria was added to gluten, while the reverse was the case in patients born after the epidemic. Under these conditions Th17 cells were the dominant producers. Thus Tc17 and Th17 responses to gluten and bacteria seem to pave the way for the chronic disease with interferon-γ-production by intraepithelial Tc1 cells and lamina propria Th1 cells. The CD associated bacteria and the dysbiosis they might cause in the resident microbiota may be a risk factor for CD either by directly influencing the immune responses in the mucosa or by enhancing inflammatory responses to gluten.
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