ArticlePloS one2018
Differential role of MyD88 and TRIF signaling in myeloid cells in the pathogenesis of autoimmune diabetes.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Lnk/Sh2b3 regulates initiation and severity of autoimmune insulitis and contributes to diabetes risk.Life science alliance · 2025Article
- Necroptosis of hippocampal neurons in paclitaxel chemotherapy-induced cognitive impairment mediates microglial activation via TLR4/MyD88 signaling pathway.Open medicine (Warsaw, Poland) · 2025Article
- Role of toll-like receptor in the pathogenesis of oral cancer.Cell biochemistry and biophysics · 2024Review
- Gut microbiota bridges the iron homeostasis and host health.Science China. Life sciences · 2023Review
- Anti-atherosclerosis mechanisms associated with regulation of non-coding RNAs by active monomers of traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Article
- Endosomal Sequestration of TLR4 Antibody Induces Myeloid-Derived Suppressor Cells and Reverses Acute Type 1 Diabetes.Diabetes · 2022Article
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Notoginsenoside R1 alleviates high glucose-induced inflammation and oxidative stress in HUVECs via upregulating miR-147a.The Kaohsiung journal of medical sciences · 2021Article
- Protein overexpression of toll-like receptor 4 and myeloid differentiation factor 88 in oral squamous cell carcinoma and clinical significance.Oncology letters · 2021Article
- 12-Lipoxygenase governs the innate immune pathogenesis of islet inflammation and autoimmune diabetes.JCI insight · 2021Article
- Crosstalk between Tryptophan Metabolism via Kynurenine Pathway and Carbohydrate Metabolism in the Context of Cardio-Metabolic Risk-Review.Journal of clinical medicine · 2021Review
- Article
- Global Deletion of the Prolactin Receptor Aggravates Streptozotocin-Induced Diabetes in Mice.Frontiers in endocrinology · 2021Article
- Exploring the Triple Interaction between the Host Genome, the Epigenome, and the Gut Microbiome in Type 1 Diabetes.International journal of molecular sciences · 2020Review
- Angiotensin II-induced hypertension and cardiac hypertrophy are differentially mediated by TLR3- and TLR4-dependent pathways.American journal of physiology. Heart and circulatory physiology · 2019Article
- Report of the Signal Transduction Society Meeting 2018-Signaling: From Past to Future.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is caused by the autoimmune destruction of the insulin-producing pancreatic beta cells. While the role of adaptive immunity has been extensively studied, the role of innate immune responses and particularly of Toll- like Receptor (TLR) signaling in T1D remains poorly understood. Here we show that myeloid cell-specific MyD88 deficiency considerably protected mice from the development of streptozotocin (STZ)-induced diabetes. The protective effect of MyD88 deficiency correlated with increased expression of the immunoregulatory enzyme indoleamine 2,3-dioxygenase (IDO) in pancreatic lymph nodes from STZ-treated mice and in bone marrow-derived dendritic cells (BMDC) stimulated with apoptotic cells. Mice with myeloid cell specific TIR-domain-containing adapter-inducing interferon-β (TRIF) knockout showed a trend towards accelerated onset of STZ-induced diabetes, while TRIF deficiency resulted in reduced IDO expression in vivo and in vitro. Moreover, myeloid cell specific MyD88 deficiency delayed the onset of diabetes in Non-Obese Diabetic (NOD) mice, whereas TRIF deficiency had no effect. Taken together, these results identify MyD88 signaling in myeloid cells as a critical pathogenic factor in autoimmune diabetes, which is antagonized by TRIF-dependent responses. This differential function of MyD88 and TRIF depends at least in part on their opposite effects in regulating IDO expression in phagocytes exposed to apoptotic cells.
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