ArticleThe Journal of clinical investigation2011
Prevention of murine autoimmune diabetes by CCL22-mediated Treg recruitment to the pancreatic islets.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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.
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Who cites it
52 citing papers in PubMed, 113 citations in OpenAlex.
- Trial
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- Islet amyloid disrupts MHC class II antigen presentation and delays autoimmune diabetes in NOD mice.Diabetologia · 2026Article
- CCL22-expressing Stem Cell-derived Islet Grafts Recruit Regulatory T Cells in Mice.Transplantation · 2026Article
- Associations of DNA methylation estimators of protein abundance with concurrent and future physical health risk factors.Scientific reports · 2025Article
- Article
- Oral exposure to PET microplastics induces the pancreatic immune response and oxidative stress in immature pigs.BMC genomics · 2025Article
- Implantation of Islets Co-Seeded with Tregs in a Novel Biomaterial Reverses Diabetes in the NOD Mouse Model.Tissue engineering and regenerative medicine · 2025Article
- Regulatory T cell dysfunction and immunotherapeutic breakthroughs in type 1 diabetes.Frontiers in endocrinology · 2025Review
- Blood immune cell profiling in adults with longstanding type 1 diabetes is associated with macrovascular complications.Frontiers in immunology · 2024Article
- A protein-based machine learning approach to the identification of inflammatory subtypes in pancreatic ductal adenocarcinoma.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2023Article
- Hypomethylation-induced regulatory programs in T cells unveiled by transcriptomic analyses.Frontiers in immunology · 2023Article
- CC Chemokine Receptor 4 (CCR4) as a Possible New Target for Therapy.International journal of molecular sciences · 2022Review
- Invariant NKT Cells Promote the Development of Highly Cytotoxic Multipotent CXCR3Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Review
- Cytokine Imprint in Preeclampsia.Frontiers in immunology · 2021Article
- AAV8 Ins1-Cre can produce efficient β-cell recombination but requires consideration of off-target effects.Scientific reports · 2020Article
- In situ recruitment of regulatory T cells promotes donor-specific tolerance in vascularized composite allotransplantation.Science advances · 2020Article
- Treg-inducing microparticles promote donor-specific tolerance in experimental vascularized composite allotransplantation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Type 1 diabetes is characterized by destruction of insulin-producing β cells in the pancreatic islets by effector T cells. Tregs, defined by the markers CD4 and FoxP3, regulate immune responses by suppressing effector T cells and are recruited to sites of action by the chemokine CCL22. Here, we demonstrate that production of CCL22 in islets after intrapancreatic duct injection of double-stranded adeno-associated virus encoding CCL22 recruits endogenous Tregs to the islets and confers long-term protection from autoimmune diabetes in NOD mice. In addition, adenoviral expression of CCL22 in syngeneic islet transplants in diabetic NOD recipients prevented β cell destruction by autoreactive T cells and thereby delayed recurrence of diabetes. CCL22 expression increased the frequency of Tregs, produced higher levels of TGF-β in the CD4+ T cell population near islets, and decreased the frequency of circulating autoreactive CD8+ T cells and CD8+ IFN-γ–producing T cells. The protective effect of CCL22 was abrogated by depletion of Tregs with a CD25-specific antibody. Our results indicate that islet expression of CCL22 recruits Tregs and attenuates autoimmune destruction of β cells. CCL22-mediated recruitment of Tregs to islets may be a novel therapeutic strategy for type 1 diabetes.
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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.