ArticleMolecular medicine (Cambridge, Mass.)2022
Increased plasmablasts enhance T cell-mediated beta cell destruction and promote the development of type 1 diabetes.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Transcriptomics of type 1 diabetes progression: a validation study in newly diagnosed patients.EBioMedicine · 2026Article
- Spatial transcriptomics from pancreas and local draining lymph node tissue reveals a lymphotoxin-β signature in human type 1 diabetes.Cell reports · 2026Article
- Mechanisms and Drug-Augmenting Strategies of Mesenchymal Stem Cells for Preserving β-Cell in Type 2 Diabetes.Drug design, development and therapy · 2026Review
- Dendritic Cells: Origin, Classification, Development, Biological Functions, and Therapeutic Potential.MedComm · 2025Review
- POU2F2 activates the Akt/mTOR signalling pathway and enhances B lymphocyte function during diabetic kidney disease by promoting PIK3CD transcription.Nephrology (Carlton, Vic.) · 2024Article
- Changes of B cell subsets in different types of diabetes and its effect on the progression of latent autoimmune diabetes in adults.Endocrine · 2024Article
- The IFIH1-A946T risk variant promotes diabetes in a sex-dependent manner.Frontiers in immunology · 2024Article
- The role of B cells in the pathogenesis of type 1 diabetes.Frontiers in immunology · 2024Review
- Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes.Scientific reports · 2023Article
- Mitochondrial redox impairment and enhanced autophagy in peripheral blood mononuclear cells from type 1 diabetic patients.Redox biology · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough type 1 diabetes (T1D) is typically described as a T cell-mediated autoimmune disease, increasing evidence for a role of B cells has emerged. However, the pivotal disease-relevant B cell subset and its contribution to islet autoimmunity remain elusive.
methodsThe frequencies and phenotypic characteristics of circulating B cell subsets were analyzed using flow cytometry in individuals with new-onset T1D, long-term T1D, type 2 diabetes, and nondiabetic controls, and also in a prospective cohort of patients receiving mesenchymal stromal cell (MSC) transplantation. NOD mice and adoptive transfer assay were used to dissect the role of the certain B cell subset in disease progression. An in-vitro coculture system of islets with immune cells was established to examine the response against islets and the underlying mechanisms.
resultsWe identified that plasmablasts, a B cell subset at the antibody-secreting stage, were significantly increased and correlated with the deterioration of beta cell function in patients with new-onset T1D. Further, a fall of plasmablast number was associated with the preservation of beta cell function in patients who received MSC transplantation after 3 months of follow-up. Meanwhile, a gradual increase of plasmablasts in pancreatic lymph nodes during the natural progression of insulitis was observed in non-obese diabetic (NOD) mice; adoptive transfer of plasmablasts together with T cells from NOD mice accelerated diabetes onset in NOD/SCID recipients.
conclusionsOur study revealed that plasmablasts may function as antigen-presenting cells and promote the activation and proinflammatory response of CD4
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