ArticleClinical immunology (Orlando, Fla.)2008
Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice.
Article in Clinical immunology (Orlando, Fla.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
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- The advent of RNA-based therapeutics for metabolic syndrome and associated conditions: a comprehensive review of the literature.Molecular biology reports · 2024Review
- Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes.Cell & bioscience · 2023Review
- The Role of Cell Organelles in Rheumatoid Arthritis with Focus on Exosomes.Biological procedures online · 2021Review
- Seeing (and Using) the Light: Recent Developments in Bioluminescence Technology.Cell chemical biology · 2020Review
- Tolerising cellular therapies: what is their promise for autoimmune disease?Annals of the rheumatic diseases · 2019Review
- Humanized Mice Reveal New Insights Into the Thymic Selection of Human Autoreactive CD8Frontiers in immunology · 2019Article
- A Mathematical Model for DC Vaccine Treatment of Type I Diabetes.Frontiers in physiology · 2019Article
- Optimal Tolerogenic Dendritic Cells in Type 1 Diabetes (T1D) Therapy: What Can We Learn From Non-obese Diabetic (NOD) Mouse Models?Frontiers in immunology · 2019Review
- Antigen Loading (e.g., Glutamic Acid Decarboxylase 65) of Tolerogenic DCs (tolDCs) Reduces Their Capacity to Prevent Diabetes in the Non-Obese Diabetes (NOD)-Severe Combined Immunodeficiency Model of Adoptive Cotransfer of Diabetes As Well As in NOD Mice.Frontiers in immunology · 2018Article
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- The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ-dependent inhibition of the AKT pathway.EMBO molecular medicine · 2016Article
- Human mesenchymal stem cells and derived extracellular vesicles induce regulatory dendritic cells in type 1 diabetic patients.Diabetologia · 2016Article
- Ablative Tumor Radiation Can Change the Tumor Immune Cell Microenvironment to Induce Durable Complete Remissions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- Inflammation and hyperglycemia mediate Deaf1 splicing in the pancreatic lymph nodes via distinct pathways during type 1 diabetes.Diabetes · 2015Article
- Enhancement of paclitaxel and carboplatin therapies by CCL2 blockade in ovarian cancers.Molecular oncology · 2014Article
- Treatment of 4T1 metastatic breast cancer with combined hypofractionated irradiation and autologous T-cell infusion.Radiation research · 2014Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week old female NOD mice have a deficit in IL-4 expression in the pancreatic lymph nodes (PLN) compared to age-matched diabetes-resistant NOD.B10 mice. By bioluminescence imaging, we demonstrated that the PLN was preferentially targeted by bone marrow-derived dendritic cells (DCs) following intravenous (IV) administration. Following IV injection of DCs transduced to express IL-4 (DC/IL-4) into 12-week old NOD mice, it was possible to significantly delay or prevent the onset of hyperglycemia. We then focused on the PLN to monitor, by microarray analysis, changes in gene expression induced by DC/IL-4 and observed a rapid normalization of the expression of many genes, that were otherwise under-expressed compared to NOD.B10 PLN. The protective effect of DC/IL-4 required both MHC and IL-4 expression by the DCs. Thus, adoptive cellular therapy, using DCs modified to express IL-4, offers an effective, tissue-targeted cellular therapy to prevent diabetes in NOD mice at an advanced stage of pre-diabetes, and may offer a safe approach to consider for treatment of high risk human pre-diabetic patients.
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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.