ArticleDiabetologia2018
A selective CD28 antagonist and rapamycin synergise to protect against spontaneous autoimmune diabetes in NOD mice.
Article in Diabetologia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Harnessing tumor immune checkpoints for autoimmune disease therapeutics.Frontiers in immunology · 2026Review
- How do immune cells shape type 1 diabetes? Insights from Mendelian randomization.Frontiers in endocrinology · 2024Article
- Advanced Delivery Strategies for Immunotherapy in Type I Diabetes Mellitus.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Review
- T regulatory cells metabolism: The influence on functional properties and treatment potential.Frontiers in immunology · 2023Review
- Personalized Immunotherapies for Type 1 Diabetes: Who, What, When, and How?Journal of personalized medicine · 2022Review
- New Developments in T Cell Immunometabolism and Therapeutic Implications for Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- Targeting co-stimulatory molecules in autoimmune disease.Nature reviews. Drug discovery · 2020Review
- Targeting Type 1 Diabetes: Selective Approaches for New Therapies.Biochemistry · 2019Review
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
Abstract
aims/hypothesisThe CD28/B7 interaction is critical for both effector T cell activation and forkhead box P3 (FOXP3)
methodsNOD mice were treated with PEGylated anti-CD28 Fab' antibody fragments (PV1-polyethylene glycol [PEG], 10 mg/kg i.p., twice weekly), rapamycin (1 mg/kg i.p., twice weekly) or a combination of both drugs. Diabetes incidence, pancreatic islet infiltration and autoreactive T cell responses were analysed.
resultsWe report that 4 week administration of PV1-PEG combined with rapamycin effectively controlled the progression of autoimmune diabetes in NOD mice at 10 weeks of age by reducing T cell activation and migration into the pancreas. Treatment with rapamycin alone was without effect, as was PV1-PEG monotherapy initiated at 4, 6 or 10 weeks of age. Prolonged PV1-PEG administration (for 10 weeks) accelerated diabetes development associated with impaired peripheral Treg homeostasis. This effect was not observed with the combined treatment. CONCLUSIONS/
interpretationCD28 antagonist and rapamycin treatment act in a complementary manner to limit T cell activation and infiltration of pancreatic islets and diabetes development. These data provide new perspectives for the treatment of autoimmune diabetes and support the therapeutic potential of protocols combining antagonists of CD28 (presently in clinical development) and the mTOR pathway.
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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.