ArticleDiabetes2012
B-cell cross-presentation of autologous antigen precipitates diabetes.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 89 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
89 citing papers in PubMed, 117 citations in OpenAlex.
- Opportunities and challenges for cancer immunotherapy based on antigen cross-presentation.Annals of medicine · 2026Review
- CD180-Associated B-Cell Alterations in Type 1 Diabetes and the In Vitro Effects of Chlorogenic Acid: An Integrated Transcriptomic and Experimental Study.International journal of molecular sciences · 2026Article
- Article
- Cross-presentation of citrullinated antigens drives cytotoxic CD8bioRxiv : the preprint server for biology · 2026Article
- The progress and perspective of nanomedicine in modulating the tumor immune microenvironment.Acta pharmaceutica Sinica. B · 2026Review
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- Stage 1 type 1 diabetes memory B lymphocytes transcriptionally differ from healthy controls and harbor insulin-binding specificities.ImmunoHorizons · 2025Article
- Activated polyreactive B cells are clonally expanded in autoantibody positive and patients with recent-onset type 1 diabetes.Cell reports · 2025Article
- Tissue Resident and Infiltrating Immune Cells: Their Influence on the Demise of Beta Cells in Type 1 Diabetes.Biomolecules · 2025Review
- Humoral immune activation within tertiary lymphoid structures is correlated with poor outcomes in oral lichen planus and lichenoid lesions.Frontiers in immunology · 2025Article
- Single-cell RNA sequencing in studies of type 1 diabetes mellitus: modern state-of-the-art and technical peculiarities.Frontiers in endocrinology · 2025Review
- The Dual Role of B Cells in the Tumor Microenvironment: Implications for Cancer Immunology and Therapy.International journal of molecular sciences · 2024Review
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Islet-antigen reactive B cells display a unique phenotype and BCR repertoire in autoantibody positive and recent-onset type 1 diabetes patients.bioRxiv : the preprint server for biology · 2024Article
- Article
- Article
- HAMSAB diet ameliorates dysfunctional signaling in pancreatic islets in autoimmune diabetes.iScience · 2024Article
- Antigen-specific T cell responses in autoimmune diabetes.Frontiers in immunology · 2024Review
- The role of B cells in the pathogenesis of type 1 diabetes.Frontiers in immunology · 2024Review
- Activated B-Cells enhance epitope spreading to support successful cancer immunotherapy.Frontiers in immunology · 2024Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For autoimmune conditions like type 1 diabetes to progress, self-reactive CD8⁺ T cells would need to interact with peptide-antigen cross-presented on the surface of antigen-presenting cells in a major histocompatibility complex (MHC) class I-restricted fashion. However, the mechanisms by which autoantigen is cross-presented remain to be identified. In this study, we show cross-presentation of islet-derived autoantigens by B cells. B cells engage self-reactive CD8⁺ T cells in the pancreatic lymph node, driving their proliferative expansion and differentiation into granzyme B⁺interferon-γ⁺lysosomal-associated membrane protein 1⁺ effector cells. B-cell cross-presentation of insulin required proteolytic cleavage and endosomal localization and was sensitive to inhibitors of protein trafficking. Absent B-cell MHC class I, or B-cell receptor restriction to an irrelevant specificity, blunted the expansion of self-reactive CD8⁺ T cells, suggesting B-cell antigen capture and presentation are critical in vivo events for CD8 activation. Indeed, the singular loss of B-cell MHC class I subverted the conversion to clinical diabetes in NOD mice, despite the presence of a pool of activated, and B cell-dependent, interleukin-21-expressing Vβ4⁺CD4⁺ T cells. Thus, B cells govern the transition from clinically silent insulitis to frank diabetes by cross-presenting autoantigen to self-reactive CD8⁺ T cells.
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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.