ArticleJournal of molecular medicine (Berlin, Germany)2010
Altered Toll-like receptor signaling pathways in human type 1 diabetes.
Article in Journal of molecular medicine (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- Identification of crucial extracellular genes as potential biomarkers in newly diagnosed Type 1 diabetesPeerJ · 2025Article
- Identification of Immune Gene Signature Associated with T Cells and Natural Killer Cells in Type 1 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- 4-Octyl itaconate attenuates glycemic deterioration by regulating macrophage polarization in mouse models of type 1 diabetes.Molecular medicine (Cambridge, Mass.) · 2023Article
- Visceral Adipose Tissue: A New Target Organ in Virus-Induced Type 1 Diabetes.Frontiers in immunology · 2021Review
- IL-27: An endogenous constitutive repressor of human monocytes.Clinical immunology (Orlando, Fla.) · 2020Article
- Mass Cytometry Studies of Patients With Autoimmune Endocrine Diseases Reveal Distinct Disease-Specific Alterations in Immune Cell Subsets.Frontiers in immunology · 2020Article
- Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes.Antioxidants & redox signaling · 2018Review
- Altered Function of Antigen-Presenting Cells in Type 1 Diabetes: A Challenge for Antigen-Specific Immunotherapy?Diabetes · 2018Review
- Article
- Blood-based signatures in type 1 diabetes.Diabetologia · 2016Review
- Polymorphisms of the Toll-Like Receptor-3 Gene in Autoimmune Adrenal Failure and Type 1 Diabetes in Polish Patients.Archivum immunologiae et therapiae experimentalis · 2016Article
- Innate inflammation in type 1 diabetes.Translational research : the journal of laboratory and clinical medicine · 2016Review
- Contrasting Roles of Islet Resident Immunoregulatory Macrophages and Dendritic Cells in Experimental Autoimmune Type 1 Diabetes.PloS one · 2016Article
- Inhibition of TLR4 attenuates vascular dysfunction and oxidative stress in diabetic rats.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Reversal of New-Onset Type 1 Diabetes With an Agonistic TLR4/MD-2 Monoclonal Antibody.Diabetes · 2015Article
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- Article
- α1-Antitrypsin therapy downregulates toll-like receptor-induced IL-1β responses in monocytes and myeloid dendritic cells and may improve islet function in recently diagnosed patients with type 1 diabetes.The Journal of clinical endocrinology and metabolism · 2014Article
- Advances in the cellular immunological pathogenesis of type 1 diabetes.Journal of cellular and molecular medicine · 2014Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is compelling evidence from animal models of type 1 diabetes (T1D) that the innate immune system plays a key role in early mechanisms triggering islet destruction. Very little is known, however, about innate immune subsets and pathways potentially involved in mechanisms leading to human T1D. The present study used a comprehensive approach to analyze innate immune functions in primary monocytes and dendritic cells (DCs) from newly diagnosed patients with T1D versus age-matched healthy individuals. We observed that incubation of PBMCs in the presence of the TLR7/8 agonist R848 led to increased proportion of plasmacytoid dendritic cells (pDCs) expressing IFN-α in patients versus healthy control subjects. We also found that TLR4 activation induced a higher frequency of IL-1β expressing monocytes and a reduction in the percentage of IL-6 expressing myeloid dendritic cells (mDCs). The altered TLR responsiveness was not due to aberrant proportions of peripheral DC subsets and monocytes in the blood and did not correlate with altered hemoglobin A1c and the expression of diabetes susceptibility genes but could potentially be associated with enhanced nuclear factor-kappa B signaling. Finally, we observed that levels of serum IFN-α2, IL-1β, IFN-γ, and CXCL-10 were elevated in new onset patients versus the control group. Taken together, our observations provide evidence that altered innate immunity exists in mDCs and pDCs from T1D and raise the possibility that these alterations may be associated with disease mechanisms.
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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.