ArticleThe Journal of clinical investigation2011
Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- A surge in serum mucosal cytokines associated with seroconversion in children at risk for type 1 diabetes.Journal of diabetes investigation · 2023Article
- Low-dose IL-2 reduces IL-21Nature communications · 2022Article
- Article
- IL-17F induces inflammation, dysfunction and cell death in mouse islets.Scientific reports · 2020Article
- Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets.Clinical & translational immunology · 2020Review
- CD122 blockade restores immunological tolerance in autoimmune type 1 diabetes via multiple mechanisms.JCI insight · 2018Article
- Interactions Between the Neuroendocrine System and T Lymphocytes in Diabetes.Frontiers in endocrinology · 2018Review
- Role of IL-21 in HTLV-1 infections with emphasis on HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).Medical microbiology and immunology · 2017Article
- Type 1 diabetes genetic susceptibility and dendritic cell function: potential targets for treatment.Journal of leukocyte biology · 2016Review
- CD4 T cell differentiation in type 1 diabetes.Clinical and experimental immunology · 2016Review
- IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis.The Journal of clinical investigation · 2015Article
- The Presence and Preferential Activation of Regulatory T Cells Diminish Adoptive Transfer of Autoimmune Diabetes by Polyclonal Nonobese Diabetic (NOD) T Cell Effectors into NSG versus NOD-scid Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Non-classical MHC I-E negatively regulates macrophage activation and Th17 cell development in NOD mice.Scientific reports · 2015Article
- Organ-specific differences in achieving tolerance.Current opinion in organ transplantation · 2015Review
- A T cell extrinsic mechanism by which IL-2 dampens Th17 differentiation.Journal of autoimmunity · 2015Article
- ROR inverse agonist suppresses insulitis and prevents hyperglycemia in a mouse model of type 1 diabetes.Endocrinology · 2015Article
- The Non-Obese Diabetic Mouse Strain as a Model to Study CD8(+) T Cell Function in Relapsing and Progressive Multiple Sclerosis.Frontiers in immunology · 2015Review
- Expression of IL-2 in β cells by AAV8 gene transfer in pre-diabetic NOD mice prevents diabetes through activation of FoxP3-positive regulatory T cells.Gene therapy · 2014Article
- Heart transplantation: challenges facing the field.Cold Spring Harbor perspectives in medicine · 2014Review
- Interleukin-21: a double-edged sword with therapeutic potential.Nature reviews. Drug discovery · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease that shows familial aggregation in humans and likely has genetic determinants. Disease linkage studies have revealed many susceptibility loci for T1D in mice and humans. The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), which has a homologous genetic interval in humans, encodes cytokine genes Il2 and Il21 and regulates diabetes and other autoimmune diseases; however, the cellular and molecular mechanisms of this regulation are still being elucidated. Here we show that T cells from NOD mice produce more Il21 and less Il2 and exhibit enhanced Th17 cell generation compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele from a diabetes-resistant mouse strain. Further, APCs from NOD and NOD.Idd3 mice played a central role in this differential Th17 cell development, and IL-21 signaling in APCs was pivotal to this process. Specifically, NOD-derived APCs showed increased production of pro-Th17 mediators and dysregulation of the retinoic acid (RA) signaling pathway compared with APCs from NOD.Idd3 and NOD.Il21r-deficient mice. These data suggest that the protective effect of the Idd3 locus is due, in part, to differential RA signaling in APCs and that IL-21 likely plays a role in this process. Thus, we believe APCs provide a new candidate for therapeutic intervention in autoimmune diseases.
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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.