ArticleDiabetes2013
Recovery from overt type 1 diabetes ensues when immune tolerance and β-cell formation are coupled with regeneration of endothelial cells in the pancreatic islets.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- The paracrine signalling between endothelial and pancreatic β-cells: implications for oxidative stress and diabetes.Journal of endocrinological investigation · 2026Review
- Single-Cell RNA Sequencing Shows Exercise ProtectsJournal of diabetes research · 2025Article
- Formation of pancreatic β-cells from precursor cells contributes to the reversal of established type 1 diabetes.Cellular immunology · 2021Article
- Drug-Integrating Amphiphilic Nanomaterial Assemblies: 1. Spatiotemporal control of cyclosporine delivery and activity using nanomicelles and nanofibrils.Journal of controlled release : official journal of the Controlled Release Society · 2021Article
- In vivo imaging of type 1 diabetes immunopathology using eye-transplanted islets in NOD mice.Diabetologia · 2019Article
- IFNγ-Induced MHC Class II Expression on Islet Endothelial Cells Is an Early Marker of Insulitis but Is Not Required for Diabetogenic CD4Frontiers in immunology · 2018Article
- The islet endothelial cell: a novel contributor to beta cell secretory dysfunction in diabetes.Diabetologia · 2017Review
- Antigen-Specific Immune Modulation Targets mTORC1 Function To Drive Chemokine Receptor-Mediated T Cell Tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Stem cell treatment for type 1 diabetes.Frontiers in cell and developmental biology · 2014Review
- Combining MK626, a novel DPP-4 inhibitor, and low-dose monoclonal CD3 antibody for stable remission of new-onset diabetes in mice.PloS one · 2014Article
- Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Immune modulation of pancreatic inflammation induces recovery from type 1 diabetes (T1D), but remission was not durable, perhaps because of an inability to sustain the formation and function of new pancreatic β-cells. We have previously shown that Ig-GAD2, carrying GAD 206-220 peptide, induced in hyperglycemic mice immune modulation that was able to control pancreatic inflammation, stimulate β-cell regeneration, and prevent T1D progression. Herein, we show that the same Ig-GAD2 regimen given to mice with overt T1D was unable to reverse the course of disease despite eradication of Th1 and Th17 cells from the pancreas. However, the regimen was able to sustain recovery from T1D when Ig-GAD2 was accompanied with transfer of bone marrow (BM) cells from healthy donors. Interestingly, alongside immune modulation, there was concomitant formation of new β-cells and endothelial cells (ECs) in the pancreas. The new β-cells were of host origin while the donor BM cells gave rise to the ECs. Moreover, transfer of purified BM endothelial progenitors instead of whole BM cells sustained both β-cell and EC formation and reversal of diabetes. Thus, overcoming T1D requires both immune modulation and repair of the islet vascular niche to preserve newly formed β-cells.
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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.