Trial reportDiabetes2008
Rapamycin monotherapy in patients with type 1 diabetes modifies CD4+CD25+FOXP3+ regulatory T-cells.
Trial report in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
73 citing papers in PubMed, 140 citations in OpenAlex.
- High-dose cholecalciferol supplementation significantly increases peripheral CD4⁺ Tregs in healthy adults without negatively affecting the frequency of other immune cells.European journal of nutrition · 2014Trial
- Rapamycin unbalances the polarization of human macrophages to M1.Immunology · 2013Trial
- Rapamycin/IL-2 combination therapy in patients with type 1 diabetes augments Tregs yet transiently impairs β-cell function.Diabetes · 2012Trial
- Fludarabine disrupts the STAT1/AhR interaction to attenuate type 1 diabetes by inducing tolerogenic dendritic cells along with targeting effector T cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- Calorie Restriction Upregulates Islet PD-L1 Signaling and Decreases the Risk of Autoimmune Diabetes Onset in NOD Mice.bioRxiv : the preprint server for biology · 2026Article
- Induction of immune education in type 1 diabetes through controlled allogeneic islet rejection at onset: a monocentric open-label pilot study.EClinicalMedicine · 2025Article
- Targeting CD4+ T Cell Glucose Metabolism: A Novel Immunotherapeutic Approach for Type 1 Diabetes.Biomolecules · 2025Review
- Immune cell senescence in autoimmunity: implications for disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2025Review
- Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions.MedComm · 2024Review
- A Stable Micellar Formulation of RAD001 for Intracerebroventricular Delivery and the Treatment of Alzheimer's Disease and Other Neurological Disorders.International journal of molecular sciences · 2023Article
- Regulatory T cells as a therapeutic approach for inflammatory bowel disease.European journal of immunology · 2023Review
- Particle-Based therapies for antigen specific treatment of type 1 diabetes.International journal of pharmaceutics · 2023Review
- Allo Beta Cell transplantation: specific features, unanswered questions, and immunological challenge.Frontiers in immunology · 2023Review
- A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives.Frontiers in immunology · 2022Review
- New Developments in T Cell Immunometabolism and Therapeutic Implications for Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- Diabetes type 1: Can it be treated as an autoimmune disorder?Reviews in endocrine & metabolic disorders · 2021Review
- Advances in Liver Transplantation: where are we in the pursuit of transplantation tolerance?European journal of immunology · 2021Review
- Tolerogenic Dendritic Cell-Based Approaches in Autoimmunity.International journal of molecular sciences · 2021Review
- Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.Cell reports · 2021Article
- Do Autism Spectrum and Autoimmune Disorders Share Predisposition Gene Signature Due to mTOR Signaling Pathway Controlling Expression?International journal of molecular sciences · 2021Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveRapamycin is an immunosuppressive drug currently used to prevent graft rejection in humans, which is considered permissive for tolerance induction. Rapamycin allows expansion of both murine and human naturally occurring CD4(+)CD25(+)FOXP3(+) T regulatory cells (nTregs), which are pivotal for the induction and maintenance of peripheral tolerance. Preclinical murine models have shown that rapamycin enhances nTreg proliferation and regulatory function also in vivo. Objective of this study was to assess whether rapamycin has in vivo effects on human nTregs. RESEARCH DESIGN AND
methodsnTreg numbers and function were examined in a unique set of patients with type 1 diabetes who underwent rapamycin monotherapy before islet transplantation.
resultsWe found that rapamycin monotherapy did not alter the frequency and functional features, namely proliferation and cytokine production, of circulating nTregs. However, nTregs isolated from type 1 diabetic patients under rapamycin treatment had an increased capability to suppress proliferation of CD4(+)CD25(-) effector T-cells compared with that before treatment.
conclusionsThese findings demonstrate that rapamycin directly affects human nTreg function in vivo, which consists of refitting their suppressive activity, whereas it does not directly change effector T-cell function.
Indexed as
Identifiers
What OpenQuestion holds
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.