ArticleFrontiers in endocrinology2020
Pancreatic Alpha-Cells Contribute Together With Beta-Cells to CXCL10 Expression in Type 1 Diabetes.
Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Clinical parameters and emerging biomarkers of partial remission in pediatric type 1 diabetes: a systematic review.Frontiers in endocrinology · 2026Pooled it
- Endotoxin Tolerance Impinges on T Cell Activation and Chemoattraction in Autoimmune Diabetes.Journal of immunology research · 2026Article
- Preclinical Diagnosis of Type 1 Diabetes: Reality or Utopia.Biomedicines · 2025Review
- Proinflammatory cytokine-induced alpha cell impairment in human islet microtissues is partially restored by dual incretin receptor agonism.Diabetologia · 2025Article
- Neutrophils in Type 1 Diabetes: Untangling the Intricate Web of Pathways and Hypothesis.Biomolecules · 2025Review
- DOC2b enrichment mitigates proinflammatory cytokine-induced CXCL10 expression by attenuating IKKβ and STAT-1 signaling in human islets.Metabolism: clinical and experimental · 2025Article
- Decoding the Significance of Alpha Cell Function in the Pathophysiology of Type 1 Diabetes.Cells · 2024Review
- The Role of Chemokines in Obesity and Exercise-Induced Weight Loss.Biomolecules · 2024Review
- Network approach reveals preferential T-cell and macrophage association with α-linked β-cells in early stage of insulitis in NOD mice.Frontiers in network physiology · 2024Article
- An Early Islet Transcriptional Signature Is Associated With Local Inflammation in Autoimmune Diabetes.Diabetes · 2023Article
- PPARs at the crossroads of T cell differentiation and type 1 diabetes.Frontiers in immunology · 2023Review
- Pancreatic Islet Cells Response to IFNγ Relies on Their Spatial Location within an Islet.Cells · 2022Article
- Whole-genome CRISPR screening identifies genetic manipulations to reduce immune rejection of stem cell-derived islets.Stem cell reports · 2022Article
- Mechanisms by Which Skeletal Muscle Myokines Ameliorate Insulin Resistance.International journal of molecular sciences · 2022Review
- Review
- Increased Expression of Viral Sensor MDA5 in Pancreatic Islets and in Hormone-Negative Endocrine Cells in Recent Onset Type 1 Diabetic Donors.Frontiers in immunology · 2022Article
- Candidate Biomarkers for the Prediction and Monitoring of Partial Remission in Pediatric Type 1 Diabetes.Frontiers in immunology · 2022Article
- Alpha cell dysfunction in type 1 diabetes is independent of a senescence program.Frontiers in endocrinology · 2022Article
- Means, Motive, and Opportunity: Do Non-Islet-Reactive Infiltrating T Cells Contribute to Autoimmunity in Type 1 Diabetes?Frontiers in immunology · 2021Review
- Chemokines in Type 1 Diabetes Mellitus.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-X-C Motif Chemokine Ligand 10 (CXCL10) is a pro-inflammatory chemokine specifically recognized by the ligand receptor CXCR3 which is mostly expressed in T-lymphocytes. Although CXCL10 expression and secretion have been widely associated to pancreatic islets both in non-obese diabetic (NOD) mice and in human type 1 diabetic (T1D) donors, the specific expression pattern among pancreatic endocrine cell subtypes has not been clarified yet. Therefore, the purpose of this study was to shed light on the pancreatic islet expression of CXCL10 in NOD, in C57Bl/6J and in NOD-SCID mice as well as in human T1D pancreata from new-onset T1D patients (DiViD study) compared to non-diabetic multiorgan donors from the INNODIA European Network for Pancreatic Organ Donors with Diabetes (EUnPOD). CXCL10 was expressed in pancreatic islets of normoglycaemic and new-onset diabetic NOD mice but not in C57Bl/6J and NOD-SCID mice. CXCL10 expression was increased in pancreatic islets of new-onset diabetic NOD mice compared to normoglycaemic NOD mice. In NOD mice, CXCL10 colocalized both with insulin and glucagon. Interestingly, CXCL10-glucagon colocalization rate was significantly increased in diabetic vs. normoglycaemic NOD mouse islets, indicating an increased expression of CXCL10 also in alpha-cells. CXCL10 was expressed in pancreatic islets of T1D patients but not in non-diabetic donors. The analysis of the expression pattern of CXCL10 in human T1D pancreata from DiViD study, revealed an increased colocalization rate with glucagon compared to insulin. Of note, CXCL10 was also expressed in alpha-cells residing in insulin-deficient islets (IDI), suggesting that CXCL10 expression in alpha cells is not driven by residual beta-cells and therefore may represent an independent phenomenon. In conclusion, we show that in T1D CXCL10 is expressed by alpha-cells both in NOD mice and in T1D patients, thus pointing to an additional novel role for alpha-cells in T1D pathogenesis and progression.
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