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FIG. 1. — Targeting B-cells mitigates autoimmune diabetes in NOD mice: what is plan B?
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Created: 2026-04-21T18:29:40
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FIG. 1.Figure 1
Model for autoantigen presentation in B-cell–depleted NOD mice. Autoantigen presentation is normally balanced between B-cells and dendritic cells (DCs) in mice ( 16 ). A : NOD autoantigen presentation. However, B-cell cognate presentation of pancreatic autoantigens may dominate in NOD mice because B-cell selection ( 17 ) and innate cell APC function are impaired ( 18 ). As a result, B-cell–driven pathogenic CD4 + T-cell expansion and effector function leads to β-cell destruction and insulin deficiency. B : Presentation without B-cells. Mature B-cell depletion in NOD mice eliminates the initiating role of B-cells in disease pathogenesis but shifts antigen presentation to other APCs that may reduce CD4 + T-cell activation in favor of Treg induction or expansion and lead to a tolerogenic state or honeymoon period without disease. C : Following B-cell reconstitution, previously induced Tregs may limit autoreactive T-cell activation and expansion, thereby enforcing long-term tolerance
▸Metadata
| pmid | ab0b8f97-7861-478a-bb45-636e03c5ccd9 |
| caption | Model for autoantigen presentation in B-cell–depleted NOD mice. Autoantigen presentation is normally balanced between B-cells and dendritic cells (DCs) in mice ( 16 ). A : NOD autoantigen presentatio |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC2699866/bin/zdb0070957820001.jpg |
| paper_title | Targeting B-cells mitigates autoimmune diabetes in NOD mice: what is plan B? |
| figure_label | FIG. 1. |
| figure_number | 1 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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