ArticleDiabetes2008
T-cell promiscuity in autoimmune diabetes.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Dual CD8 and TCR editing in regulatory T cells mediates HLA-A2-restricted tissue-specific homing.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Correction of T-Cell Repertoire and Autoimmune Diabetes in NOD Mice by Non-myeloablative T-Cell Depleted Allogeneic HSCT.Stem cells translational medicine · 2023Article
- Analysis of tumor infiltrating CD4+ and CD8+ CDR3 sequences reveals shared features putatively associated to the anti-tumor immune response.Frontiers in immunology · 2023Article
- Noncontiguous T cell epitopes in autoimmune diabetes: From mice to men and back again.The Journal of biological chemistry · 2021Review
- Nature of T cell epitopes in lupus antigens and HLA-DR determines autoantibody initiation and diversification.Annals of the rheumatic diseases · 2019Article
- T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.Frontiers in endocrinology · 2017Review
- High-throughput sequencing reveals restricted TCR Vβ usage and public TCRβ clonotypes among pancreatic lymph node memory CD4(+) T cells and their involvement in autoimmune diabetes.Molecular immunology · 2016Article
- Mechanisms of autoimmunity in the non-obese diabetic mouse: effector/regulatory cell equilibrium during peak inflammation.Immunology · 2016Review
- Generation of β cell-specific human cytotoxic T cells by lentiviral transduction and their survival in immunodeficient human leucocyte antigen-transgenic mice.Clinical and experimental immunology · 2015Article
- Compensatory mechanisms allow undersized anchor-deficient class I MHC ligands to mediate pathogenic autoreactive T cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Epitope-specificity of recombinant antibodies reveals promiscuous peptide-binding properties.Protein science : a publication of the Protein Society · 2012Article
- T cell populations in the pancreatic lymph node naturally and consistently expand and contract in NOD mice as disease progresses.Molecular immunology · 2012Article
- Article
- Spectratyping analysis of the islet-reactive T cell repertoire in diabetic NOD Igμ(null) mice after polyclonal B cell reconstitution.Journal of translational medicine · 2011Article
- Cumulative autoimmunity: T cell clones recognizing several self-epitopes exhibit enhanced pathogenicity.Frontiers in immunology · 2011Article
- Central nervous system destruction mediated by glutamic acid decarboxylase-specific CD4+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Suppression of ongoing T cell-mediated autoimmunity by peptide-MHC class II dimer vaccination.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveIt is well established that the primary mediators of beta-cell destruction in type 1 diabetes are T-cells. Nevertheless, the molecular basis for recognition of beta-cell-specific epitopes by pathogenic T-cells remains ill defined; we seek to further explore this issue. RESEARCH DESIGN AND
methodsTo determine the properties of beta-cell-specific T-cell receptors (TCRs), we characterized the fine specificity, functional and relative binding avidity/affinity, and diabetogenicity of a panel of GAD65-specific CD4(+) T-cell clones established from unimmunized 4- and 14-week-old NOD female mice.
resultsThe majority of GAD65-specific CD4(+) T-cells isolated from 4- and 14-week-old NOD female mice were specific for peptides spanning amino acids 217-236 (p217) and 290-309 (p290). Surprisingly, 31% of the T-cell clones prepared from 14-week-old but not younger NOD mice were stimulated with both p217 and p290. These promiscuous T-cell clones recognized the two epitopes when naturally processed and presented, and this dual specificity was mediated by a single TCR. Furthermore, promiscuous T-cell clones demonstrated increased functional avidity and relative TCR binding affinity, which correlated with enhanced islet infiltration on adoptive transfer compared with that of monospecific T-cell clones.
conclusionsThese results indicate that promiscuous recognition contributes to the development of GAD65-specific CD4(+) T-cell clones in NOD mice. Furthermore, these findings suggest that T-cell promiscuity reflects a novel form of T-cell avidity maturation.
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.