ArticleDiabetes2014
IRAK-M deficiency promotes the development of type 1 diabetes in NOD mice.
Article in Diabetes, 2014. 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
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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
18 citing papers in PubMed, 27 citations in OpenAlex.
- Masterful macrophages: understanding and targeting activation dysfunction in diabetic wounds.Burns & trauma · 2025Review
- Pharmacological insights and role of bufalin (bufadienolides) in inflammation modulation: a narrative review.Inflammopharmacology · 2024Review
- Interleukin-1 receptor-associated kinase 2 promotes inflammatory reactions by activating the nuclear factor kappa-B signaling pathway in diabetic nephropathy.Central-European journal of immunology · 2023Article
- Changes in plasma IRAK-M in patients with prediabetes and its relationship with related metabolic indexes: a cross-sectional study.The Journal of international medical research · 2022Article
- IL-1R-IRAKM-Slc25a1 signaling axis reprograms lipogenesis in adipocytes to promote diet-induced obesity in mice.Nature communications · 2022Article
- Cathelicidin-related antimicrobial peptide protects against enteric pathogen-accelerated type 1 diabetes in mice.Theranostics · 2022Article
- Article
- IRAK-M knockout promotes allergic airway inflammation, but not airway hyperresponsiveness, in house dust mite-induced experimental asthma model.Journal of thoracic disease · 2021Article
- Mitochondrial dysfunction and pancreatic islet β-cell failure (Review).Experimental and therapeutic medicine · 2020Review
- Evaluation of an HMGA2 variant for pleiotropic effects on height and metabolic traits in ponies.Journal of veterinary internal medicine · 2019Article
- Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation.Journal of leukocyte biology · 2018Review
- Molecular Mechanisms of T Cells Activation by Dendritic Cells in Autoimmune Diseases.Frontiers in pharmacology · 2018Review
- IRAK-M Deficiency Exacerbates Ischemic Neurovascular Injuries in Experimental Stroke Mice.Frontiers in cellular neuroscience · 2018Article
- Critical Role of IRAK-M in Regulating Antigen-Induced Airway Inflammation.American journal of respiratory cell and molecular biology · 2017Article
- Increased translocation of antigens to endosomes and TLR4 mediated endosomal recruitment of TAP contribute to nicotine augmented cross-presentation.Oncotarget · 2016Article
- The importance of the Non Obese Diabetic (NOD) mouse model in autoimmune diabetes.Journal of autoimmunity · 2016Review
- The role of Interleukin Receptor Associated Kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction.Journal of molecular and cellular cardiology · 2015Article
- A novel "humanized mouse" model for autoimmune hepatitis and the association of gut microbiota with liver inflammation.Hepatology (Baltimore, Md.) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Type 1 diabetes mellitus (T1DM) is an organ-specific autoimmune disease characterized by progressive destruction of insulin-secreting pancreatic β-cells. Both T-cell-mediated adaptive responses as well as innate immune processes are involved in pathogenesis. Interleukin-1 receptor-associated kinase M (IRAK-M) can effectively inhibit the MyD88 downstream signals in Toll-like receptor pathways, while lack of IRAK-M is known to be associated with autoimmunity. Our study showed that IRAK-M-deficient (IRAK-M(-/-)) nonobese diabetic (NOD) mice displayed early onset and rapid progression of T1DM with impaired glucose tolerance, more severe insulitis, and increased serum anti-insulin autoantibodies. Mechanistic studies showed that the enhanced activation and antigen-presenting function of IRAK-M(-/-) antigen-presenting cells from IRAK-M(-/-) mice were responsible for the rapid progression of disease. Moreover, IRAK-M(-/-) dendritic cells induced enhanced activation of diabetogenic T cells in vitro and the rapid onset of T1DM in vivo in immunodeficient NOD mice when cotransferred with diabetogenic T cells. This study illustrates how the modulation of innate immune pathways through IRAK-M influences the development of autoimmune diabetes.
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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.