ArticleDiabetes2010
Invariant natural killer T-cell control of type 1 diabetes: a dendritic cell genetic decision of a silver bullet or Russian roulette.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Single-cell antigen receptor sequencing in pigs with influenza.Communications biology · 2025Article
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Review
- Unaltered influenza disease outcomes in swine prophylactically treated with α-galactosylceramide.Developmental and comparative immunology · 2021Article
- CD70 Inversely Regulates Regulatory T Cells and Invariant NKT Cells and Modulates Type 1 Diabetes in NOD Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Two to Tango: Dialogue between Adaptive and Innate Immunity in Type 1 Diabetes.Journal of diabetes research · 2020Review
- CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism.Scientific reports · 2018Article
- Interferon-γ Limits Diabetogenic CD8Diabetes · 2017Article
- Mouse Invariant Monoclonal Antibody NKT14: A Novel Tool to Manipulate iNKT Cell Function In Vivo.PloS one · 2015Article
- Invariant Natural Killer T Cells are Reduced in Hereditary Hemochromatosis Patients.Journal of clinical immunology · 2015Article
- Real-time immune cell interactions in target tissue during autoimmune-induced damage and graft tolerance.The Journal of experimental medicine · 2014Article
- Genetic and Pharmacologic Models for Type 1 Diabetes.Current protocols in mouse biology · 2013Article
- Mice deficient in CD38 develop an attenuated form of collagen type II-induced arthritis.PloS one · 2012Article
- The split personality of NKT cells in malignancy, autoimmune and allergic disorders.Immunotherapy · 2011Review
- Unmasking genes in a type 1 diabetes-resistant mouse strain that enhances pathogenic CD8 T-cell responses.Diabetes · 2011Article
- Stimulation of a shorter duration in the state of anergy by an invariant natural killer T cell agonist enhances its efficiency of protection from type 1 diabetes.Clinical and experimental immunology · 2011Article
- Invariant natural killer T cells: bridging innate and adaptive immunity.Cell and tissue research · 2011Review
- Natural killer T cells in health and disease.Frontiers in bioscience (Scholar edition) · 2011Review
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- Advances and challenges in biomarker development for type 1 diabetes prediction and prevention using omic technologies.Expert opinion on medical diagnostics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveIn part, activation of invariant natural killer T (iNKT)-cells with the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the development of T-cell-mediated autoimmune type 1 diabetes in NOD mice by inducing the downstream differentiation of antigen-presenting dendritic cells (DCs) to an immunotolerogenic state. However, in other systems iNKT-cell activation has an adjuvant-like effect that enhances rather than suppresses various immunological responses. Thus, we tested whether in some circumstances genetic variation would enable activated iNKT-cells to support rather than inhibit type 1 diabetes development. RESEARCH DESIGN AND
methodsWe tested whether iNKT-conditioned DCs in NOD mice and a major histocompatibility complex-matched C57BL/6 (B6) background congenic stock differed in capacity to inhibit type 1 diabetes induced by the adoptive transfer of pathogenic AI4 CD8 T-cells.
resultsUnlike those of NOD origin, iNKT-conditioned DCs in the B6 background stock matured to a state that actually supported rather than inhibited AI4 T-cell-induced type 1 diabetes. The induction of a differing activity pattern of T-cell costimulatory molecules varying in capacity to override programmed death-ligand-1 inhibitory effects contributes to the respective ability of iNKT-conditioned DCs in NOD and B6 background mice to inhibit or support type 1 diabetes development. Genetic differences inherent to both iNKT-cells and DCs contribute to their varying interactions in NOD and B6.H2(g7) mice.
conclusionsThis great variability in the interactions between iNKT-cells and DCs in two inbred mouse strains should raise a cautionary note about considering manipulation of this axis as a potential type 1 diabetes prevention therapy in genetically heterogeneous humans.
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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.