ReviewJournal of autoimmunity2016
Antigen presentation events during the initiation of autoimmune diabetes in the NOD mouse.
Review in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Multiomics approaches reveal direct NF-κB p65 target genes in pancreatic islets during cytokine exposure and in type 1 diabetes.American journal of physiology. Endocrinology and metabolism · 2026Article
- c-MYC enhances transcription of the type 1 diabetes mellitus associated gene BATF3 via promoter binding.Scientific reports · 2026Article
- RIPK1 regulates β-cell fate via actions on gene expression and kinase signaling in a mouse model of β-cell self-reactivity.Cell death & disease · 2026Article
- Metformin prevents diabetes development in type 1 diabetes models via suppression of mTOR and STAT3 signaling in immune cells.Scientific reports · 2025Article
- The insulin secretory granule is a hotspot for autoantigen formation in type 1 diabetes.Diabetologia · 2024Review
- Mechanistic Insights into Immune-Microbiota Interactions and Preventive Role of Probiotics Against Autoimmune Diabetes Mellitus.Probiotics and antimicrobial proteins · 2023Review
- Tolerogenic dendritic cells in type 1 diabetes: no longer a concept.Frontiers in immunology · 2023Review
- Transcriptional re-programming of insulin B-chain epitope-specific T-follicular helper cells into anti-diabetogenic T-regulatory type-1 cells.Frontiers in immunology · 2023Article
- Sustained high glucose intake accelerates type 1 diabetes in NOD mice.Frontiers in endocrinology · 2022Article
- Revisiting the Antigen-Presenting Function of β Cells in T1D Pathogenesis.Frontiers in immunology · 2021Review
- Regulatory B Cells in Type 1 Diabetes.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Anti-Inflammatory and Pro-Autophagy Effects of the Cannabinoid Receptor CB2R: Possibility of Modulation in Type 1 Diabetes.Frontiers in pharmacology · 2021Review
- Evolving Antibody Therapies for the Treatment of Type 1 Diabetes.Frontiers in immunology · 2020Review
- Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.Cell reports · 2019Article
- HLA-B*39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Autoreactive T cells in type 1 diabetes.The Journal of clinical investigation · 2017Review
- miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes.Cellular & molecular immunology · 2017Review
- Beyond Genetics: What Causes Type 1 Diabetes.Clinical reviews in allergy & immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
This is a brief summary of our studies of NOD autoimmune diabetes examining the events during the initial stage of the process. Our focus has been on antigen presentation events and the antigen presenting cells (APC) inside islets. Islets of non-diabetic mice contain resident macrophages that are developmentally distinct from those in the inter-acinar stroma. The autoimmune process starts with the entrance of CD4+ T cells together with a burst of a subset of dendritic cells (DC) bearing CD103. The CD103+ DC develop under the influence of the Batf3 transcription factor. Batf3 deficient mice do not develop diabetes and their islets are uninfiltrated throughout life. Thus, the CD103+ DC are necessary for the progression of autoimmune diabetes. The major CD4+ T cell response in NOD are the T cells directed to insulin. In particular, the non-conventional 12-20 segment of the insulin B chain is presented by the class II MHC molecule I-A(g7) and elicits pathogenic CD4+ T cells. We discuss that the diabetic process requires the CD103+ DC, the CD4+ T cells to insulin peptides, and NOD specific I-Ag(7) MHC-II allele. Finally, our initial studies indicate that beta cells transfer insulin containing vesicles to the local APC in a contact-dependent reaction. Live images of beta cells interactions with the APC and electron micrographs of islet APCs also show the transfer of granules.
Indexed as
Identifiers
What OpenQuestion holds
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.