ArticleDiabetologia2018
IFN-α induces a preferential long-lasting expression of MHC class I in human pancreatic beta cells.
Article in Diabetologia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Molecular Footprints of the Immune Assault on Pancreatic Beta Cells in Type 1 Diabetes.Frontiers in endocrinology · 2020Pooled it
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- The β-cells in type 1 diabetes mellitus: findings from human pancreas studies.Nature reviews. Endocrinology · 2026Review
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- Long-term major histocompatibility complex class I suppression in astronauts and clinical implications.Communications biology · 2026Review
- Autoimmunity and peginterferon therapy for polycythemia vera.HemaSphere · 2026Review
- Single-cell RNA sequencing of terminal ileal biopsies identifies signatures of Crohn's disease pathogenesis.Nature genetics · 2026Article
- Real-time in vivo analysis of murine β cells reveals autophagic flux defects before onset of autoimmune diabetes.Science translational medicine · 2026Article
- Type I Interferons as Contextual Regulators of B-Cell Tolerance in Type 1 Diabetes.Biomolecules · 2026Review
- Dual roles for influenza A protein PA-X: limiting inflammatory response and disrupting MHC I antigen presentation in human respiratory epithelium.bioRxiv : the preprint server for biology · 2026Article
- A single-cell transcriptomic landscape characterizes the endocrine system aging in the mouse.Protein & cell · 2026Article
- Immunological profiling of rheumatoid factor-positive primary Sjögren's syndrome by single-cell RNA sequencing.Frontiers in immunology · 2026Article
- IFNβ-pSTAT1-IRF1 axis controls colorectal tumor development through induction of immunogenic Ly6CNeoplasia (New York, N.Y.) · 2026Article
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- Type 1 diabetes mellitus prevention: present and future.Nature reviews. Endocrinology · 2025Review
- Review of Promising Off-Label Use of Deucravacitinib.International journal of molecular sciences · 2025Review
- Single-cell transcriptomics uncovers key immune drivers of vaccine efficacy in cattle.BMC genomics · 2025Article
- IFN-α Neutralizing Antibodies Distinguish LADA From Early-onset Type 1 Diabetes.The Journal of clinical endocrinology and metabolism · 2025Article
- Pharmacological inhibition of tyrosine protein-kinase 2 reduces islet inflammation and delays type 1 diabetes onset in mice.EBioMedicine · 2025Article
- Enterovirus VP1 protein and HLA class I hyperexpression in pancreatic islet cells of organ donors with type 1 diabetes.Diabetologia · 2025Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
aims/hypothesisIFN-α, a cytokine expressed in human islets from individuals affected by type 1 diabetes, plays a key role in the pathogenesis of diabetes by upregulating inflammation, endoplasmic reticulum (ER) stress and MHC class I overexpression, three hallmarks of islet histology in early type 1 diabetes. We tested whether expression of these mediators of beta cell loss is reversible upon IFN-α withdrawal or IFN-α pathway inhibition.
methodsIFN-α-induced MHC class I overexpression, ER stress and inflammation were evaluated by flow cytometry, immunofluorescence and real-time PCR in human EndoC-βH1 cells or human islets exposed to IFN-α with or without the presence of Janus kinase (JAK) inhibitors. Protein expression was evaluated by western blot.
resultsIFN-α-induced expression of inflammatory and ER stress markers returned to baseline after 24-48 h following cytokine removal. In contrast, MHC class I overexpression at the cell surface persisted for at least 7 days. Treatment with JAK inhibitors, when added with IFN-α, prevented MHC class I overexpression, but when added 24 h after IFN-α exposure these inhibitors failed to accelerate MHC class I return to baseline. CONCLUSIONS/
interpretationIFN-α mediates a long-lasting and preferential MHC class I overexpression in human beta cells, which is not affected by the subsequent addition of JAK inhibitors. These observations suggest that IFN-α-stimulated long-lasting MHC class I expression may amplify beta cell antigen presentation during the early phase of type 1 diabetes and that IFN-α inhibitors might need to be used at very early stages of the disease to be effective.
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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.