ArticleDiabetologia2013
Double deficiency in IL-17 and IFN-γ signalling significantly suppresses the development of diabetes in the NOD mouse.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Changes of Regulatory T Cells and of Proinflammatory and Immunosuppressive Cytokines in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.Journal of diabetes research · 2016Pooled it
- Analysis of the frequency of single nucleotide polymorphisms in cytokine genes in patients with New Onset Diabetes After Transplant.Scientific reports · 2021Trial
- Essential role of interferon-regulatory factor 4 in regulating diabetogenic CD4+ T and innate immune cells in autoimmune diabetes in NOD mice.Clinical and experimental immunology · 2025Article
- Causal Relationship Between Type 2 Diabetes Mellitus and Preeclampsia: A Bidirectional Two-Sample Mendelian Randomized Study.International journal of women's health · 2025Article
- Single-cell analysis reveals islet autoantigen's immune activation in type 1 diabetes patients.Journal of clinical biochemistry and nutrition · 2025Article
- Impact of hyperglycemia on immune cell function: a comprehensive review.Diabetology international · 2024Review
- TYK2 signaling promotes the development of autoreactive CD8Nature communications · 2024Article
- Article
- Clonally expanded, thyrotoxic effector CD8Science translational medicine · 2023Article
- PPARs at the crossroads of T cell differentiation and type 1 diabetes.Frontiers in immunology · 2023Review
- Role of the adaptive immune system in diabetic kidney disease.Journal of diabetes investigation · 2022Review
- T cell transgressions: Tales of T cell form and function in diverse disease states.International reviews of immunology · 2022Review
- Ursolic acid regulates gut microbiota and corrects the imbalance of Th17/Treg cells in T1DM rats.PloS one · 2022Article
- Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice.Frontiers in pharmacology · 2022Article
- T helper 17 cells: A new actor on the stage of type 2 diabetes and aging?Journal of diabetes investigation · 2021Review
- IL-17A is involved in diabetic inflammatory pathogenesis by its receptor IL-17RA.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Epigenetic modulation of selected immune response genes and altered functions of T lymphocytes and macrophages collectively contribute to autoimmune diabetes protection.BBA advances · 2021Article
- Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.PloS one · 2021Article
- Lipid deposition and metaflammation in diabetic kidney disease.Current opinion in pharmacology · 2020Review
- IL-17F induces inflammation, dysfunction and cell death in mouse islets.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisT helper type (Th) 17 cells have been shown to play important roles in mouse models of several autoimmune diseases that have been classified as Th1 diseases. In the NOD mouse, the relevance of Th1 and Th17 is controversial, because single-cytokine-deficient NOD mice develop diabetes similarly to wild-type NOD mice.
methodsWe studied the impact of IL-17/IFN-γ receptor double deficiency in NOD mice on the development of insulitis/diabetes compared with IL-17 single-deficient mice and wild-type mice by monitoring diabetes-related phenotypes. The lymphocyte phenotypes were determined by flow cytometric analysis.
resultsIL-17 single-deficient NOD mice showed delayed onset of diabetes and reduced severity of insulitis, but the cumulative incidence of longstanding diabetes in the IL-17-deficient mice was similar to that in wild-type mice. The IL-17/IFN-γ receptor double-deficient NOD mice showed an apparent decline in longstanding diabetes onset, but not in insulitis compared with that in the IL-17 single-deficient mice. We also found that double-deficient NOD mice had a severe lymphopenic phenotype and preferential increase in regulatory T cells among CD4(+) T cells compared with the IL-17 single-deficient mice and wild-type NOD mice. An adoptive transfer study with CD4(+)CD25(-) T cells from young non-diabetic IL-17 single-deficient NOD mice, but not those from older mice, showed significantly delayed disease onset in immune-deficient hosts compared with the corresponding wild-type mice. CONCLUSIONS/
interpretationThese results indicate that IL-17/Th17 participates in the development of insulitis and that both IL-17 and IFN-γ signalling may synergistically contribute to the development of diabetes in NOD mice.
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.