ArticleDiabetes2015
DCIR2+ cDC2 DCs and Zbtb32 Restore CD4+ T-Cell Tolerance and Inhibit Diabetes.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 65 citations in OpenAlex.
- Recombinant Antibody Vaccines for Targeted Antigen Delivery: Design Principles and Immunological Applications.Vaccines · 2026Review
- Tunable wrinkled topographies direct dendritic cell maturation and immune phenotypes.Acta biomaterialia · 2026Article
- STING/type I interferon pathway is required for antigen-containing PLGA nanoparticle- and apoptotic cell-induced CD4+ T cell tolerance.Science advances · 2026Article
- Taming autoimmune thyroiditis: cellular immunomodulation through MSCs, Tregs, and tolDCs.Frontiers in immunology · 2026Review
- Low-dose allergen targeting to cDC2 induces long-term protection associated with induction of regulatory-like IL-10Frontiers in immunology · 2026Article
- Dendritic Cells: Origin, Classification, Development, Biological Functions, and Therapeutic Potential.MedComm · 2025Review
- Article
- Functional Specialization and Collaboration of cDC2 Subsets in CD4+ T Cell Priming and Differentiation.Immunological reviews · 2025Review
- Role of USP7 in the regulation of tolerogenic dendritic cell function in type 1 diabetes.Cellular & molecular biology letters · 2025Article
- Multi-omics insights into the pathogenesis of diabetic cardiomyopathy: epigenetic and metabolic profiles.Epigenomics · 2025Article
- Emerging T cell immunoregulatory mechanisms in multiple sclerosis and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Antigen-specific T cell responses in autoimmune diabetes.Frontiers in immunology · 2024Review
- The Application of Nanovaccines in Autoimmune Diseases.International journal of nanomedicine · 2024Review
- Epitope-based precision immunotherapy of Type 1 diabetes.Human vaccines & immunotherapeutics · 2023Article
- Dendritic cell immunoreceptor 2 (DCIR2) deficiency decreases hepatic conventional dendritic cell content but not the progression of diet-induced obesity.Immunity, inflammation and disease · 2023Article
- TIM-3 increases the abundance of type-2 dendritic cells during Leishmania donovani infection by enhancing IL-10 production via STAT3.Cell death & disease · 2023Article
- Dendritic cell marker Clec4a4 deficiency limits atherosclerosis progression.Atherosclerosis plus · 2023Article
- Life and death of tolerogenic dendritic cells.Trends in immunology · 2023Review
- Targeted delivery of autoantigen to dendritic cells prevents development of spontaneous uveitis.Frontiers in immunology · 2023Article
- Tolerogenic dendritic cells in type 1 diabetes: no longer a concept.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
During autoimmunity, the normal ability of dendritic cells (DCs) to induce T-cell tolerance is disrupted; therefore, autoimmune disease therapies based on cell types and molecular pathways that elicit tolerance in the steady state may not be effective. To determine which DC subsets induce tolerance in the context of chronic autoimmunity, we used chimeric antibodies specific for DC inhibitory receptor 2 (DCIR2) or DEC-205 to target self-antigen to CD11b(+) (cDC2) DCs and CD8(+) (cDC1) DCs, respectively, in autoimmune-prone nonobese diabetic (NOD) mice. Antigen presentation by DCIR2(+) DCs but not DEC-205(+) DCs elicited tolerogenic CD4(+) T-cell responses in NOD mice. β-Cell antigen delivered to DCIR2(+) DCs delayed diabetes induction and induced increased T-cell apoptosis without interferon-γ (IFN-γ) or sustained expansion of autoreactive CD4(+) T cells. These divergent responses were preceded by differential gene expression in T cells early after in vivo stimulation. Zbtb32 was higher in T cells stimulated with DCIR2(+) DCs, and overexpression of Zbtb32 in T cells inhibited diabetes development, T-cell expansion, and IFN-γ production. Therefore, we have identified DCIR2(+) DCs as capable of inducing antigen-specific tolerance in the face of ongoing autoimmunity and have also identified Zbtb32 as a suppressive transcription factor that controls T cell-mediated autoimmunity.
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.