ArticleFrontiers in immunology2018
Increased iNKT17 Cell Frequency in the Intestine of Non-Obese Diabetic Mice Correlates With High
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Gut Microbiota and Autoimmune Diseases: The Therapeutic Potential of Probiotics.Current microbiology · 2026Review
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- Article
- Considerations for Gut Microbiota and Probiotics in Patients with Diabetes Amidst the Covid-19 Pandemic: A Narrative Review.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2020Review
- Evaluating the Causal Role of Gut Microbiota in Type 1 Diabetes and Its Possible Pathogenic Mechanisms.Frontiers in endocrinology · 2020Review
- The imbalance of gut microbiota and its correlation with plasma inflammatory cytokines in pemphigus vulgaris patients.Scandinavian journal of immunology · 2019Article
- Exploiting the Zonulin Mouse Model to Establish the Role of Primary Impaired Gut Barrier Function on Microbiota Composition and Immune Profiles.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
iNKT cells play different immune function depending on their cytokine-secretion phenotype. iNKT17 cells predominantly secrete IL-17 and have an effector and pathogenic role in the pathogenesis of autoimmune diseases such as type 1 diabetes (T1D). In line with this notion, non-obese diabetic (NOD) mice that spontaneously develop T1D have an increased percentage of iNKT17 cells compared to non-autoimmune strains of mice. The factors that regulate iNKT cell expansion and acquisition of a specific iNKT17 cell phenotype are unclear. Here, we demonstrate that the percentage of iNKT17 cells is increased in the gut more than peripheral lymphoid organs of NOD mice, thus suggesting that the intestinal environment promotes iNKT17 cell differentiation in these mice. Increased intestinal iNKT17 cell differentiation in NOD mice is associated with the presence of pro-inflammatory IL-6-secreting dendritic cells that could contribute to iNKT cell expansion and iNKT17 cell differentiation. In addition, we found that increased iNKT17 cell differentiation in the large intestine of NOD mice is associated with a specific gut microbiota profile. We demonstrated a positive correlation between percentage of intestinal iNKT17 cells and bacterial strain richness (α-diversity) and relative abundance of
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.