ReviewCurrent opinion in immunology2011
CD4 T cells and their antigens in the pathogenesis of autoimmune diabetes.
Review in Current opinion in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
- Review
- Fluvoxamine inhibits Th1 and Th17 polarization and function by repressing glycolysis to attenuate autoimmune progression in type 1 diabetes.Molecular medicine (Cambridge, Mass.) · 2024Article
- Islet beta-cells and intercellular adhesion molecule-1 (ICAM-1): Integrating immune responses that influence autoimmunity and graft rejection.Autoimmunity reviews · 2023Review
- Astilbin Activates the Reactive Oxidative Species/PPARγ Pathway to Suppress Effector CD4Frontiers in pharmacology · 2022Article
- MBD2 acts as a repressor to maintain the homeostasis of the Th1 program in type 1 diabetes by regulating the STAT1-IFN-γ axis.Cell death and differentiation · 2022Article
- Mitochondria Transfer to CD4Immunometabolism · 2022Article
- Immunological balance between Treg and Th17 lymphocytes as a key element of type 1 diabetes progression in children.Frontiers in immunology · 2022Article
- Lymphotoxins Serve as a Novel Orchestrator in T1D Pathogenesis.Frontiers in immunology · 2022Review
- Article
- A Single L/D-Substitution at Q4 of the mInsAFrontiers in immunology · 2021Article
- Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes.Diabetologia · 2020Article
- CD19+IgM+ cells demonstrate enhanced therapeutic efficacy in type 1 diabetes mellitus.JCI insight · 2018Article
- Altered homeostasis and development of regulatory T cell subsets represent an IL-2R-dependent risk for diabetes in NOD mice.Science signaling · 2017Article
- T cells display mitochondria hyperpolarization in human type 1 diabetes.Scientific reports · 2017Article
- Subtyping of Type 1 Diabetes as Classified by Anti-GAD Antibody, IgE Levels, and Tyrosine kinase 2 (TYK2) Promoter Variant in the Japanese.EBioMedicine · 2017Article
- Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex.Frontiers in endocrinology · 2017Review
- Downregulation of cathepsin G reduces the activation of CD4+ T cells in murine autoimmune diabetes.American journal of translational research · 2017Article
- Anti-inflammatory activity of chloroquine and amodiaquine through p21-mediated suppression of T cell proliferation and Th1 cell differentiation.Biochemical and biophysical research communications · 2016Article
- Metabolism of murine TH 17 cells: Impact on cell fate and function.European journal of immunology · 2016Review
- Pathogenic T helper type 17 cells contribute to type 1 diabetes independently of interleukin-22.Clinical and experimental immunology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Pathogenesis of type 1 diabetes (T1D) is mediated by effector T cells and CD4 Th1 and Th17T cells have important roles in this process. While effector function of Th1 cells is well established, because of their inherent plasticity Th17 cells have been more controversial. Th17 cells contribute to pathogenicity, but several studies indicate that Th17 cells transfer disease through conversion to Th1 cells in vivo. CD4T cells are attracted to islets by β-cell antigens which include insulin and the two new autoantigens, chromogranin A and islet amyloid polypeptide, all proteins of the secretory granule. Peptides of insulin and ChgA bind to the NOD class II molecule in an unconventional manner and since autoantigenic peptides may typically bind to MHC with low affinity, it is postulated that post-translational modifications of β-cell peptides could contribute to the interaction between peptides, MHC, and the autoreactive TCR.
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.