ArticleEMBO molecular medicine2014
Macrophages and β-cells are responsible for CXCR2-mediated neutrophil infiltration of the pancreas during autoimmune diabetes.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Diabetes Mellitus Facilitates Gallstone Formation Through CXCR2-NETs-Mediated Liver-Bile Barrier Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Effects of CXCR1/2 Blockade with Ladarixin on Streptozotocin-Induced Type 1 Diabetes Mellitus and Peripheral Neuropathy and Retinopathy in Rat.Diabetes & metabolism journal · 2025Article
- NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.Journal of neuroinflammation · 2025Article
- Scaffold-free endocrine tissue engineering: role of islet organization and implications in type 1 diabetes.BMC endocrine disorders · 2025Review
- Neutrophils in Type 1 Diabetes: Untangling the Intricate Web of Pathways and Hypothesis.Biomolecules · 2025Review
- Beyond inflammation: the multifaceted therapeutic potential of targeting the CXCL8-CXCR1/2 axis in type 1 diabetes.Frontiers in immunology · 2025Review
- NETs: a new target for autoimmune disease.Frontiers in immunology · 2025Review
- 4-Phenyl Butyric Acid (4-PBA) Suppresses Neutrophil Recruitment in a Murine Model of Acute Perinatal Inflammation.Journal of immunology research · 2025Article
- Not just sugar: metabolic control of neutrophil development and effector functions.Journal of leukocyte biology · 2024Review
- The immunology of type 1 diabetes.Nature reviews. Immunology · 2024Review
- GαJournal of the Endocrine Society · 2024Article
- The N-Methyl-D-Aspartate Receptor Antagonist Dextromethorphan Improves Glucose Homeostasis and Preserves Pancreatic Islets in NOD Mice.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2024Article
- Functional screening and rational design of compounds targeting GPR132 to treat diabetes.Nature metabolism · 2023Article
- Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023Review
- Bioinformatic Analysis of the CXCR2 Ligands in Cancer Processes.International journal of molecular sciences · 2023Article
- Macrophage: Key player in the pathogenesis of autoimmune diseases.Frontiers in immunology · 2023Review
- Macrophages and neutrophils are necessary for ER stress-induced β cell loss.Cell reports · 2022Article
- The Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Oral Cavity and Abdominal Organs.International journal of molecular sciences · 2022Review
- Neutrophils Actively Contribute to Obesity-Associated Inflammation and Pathological Complications.Cells · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune type 1 diabetes (T1D) development results from the interaction between pancreatic β-cells, and the innate and the adaptive immune systems culminating with the destruction of the insulin-secreting β-cells by autoreactive T cells. This diabetogenic course starts during the first postnatal weeks by the infiltration of the pancreatic islets by innate immune cells and particularly neutrophils. Here, we aim to determine the cellular and molecular mechanism leading to the recruitment of this neutrophils in the pancreatic islets of non-obese diabetic (NOD) mice. Here, we show that neutrophil recruitment in the pancreatic islets is controlled by inflammatory macrophages and β-cells themselves. Macrophages and β-cells produce the chemokines CXCL1 and CXCL2, recruiting CXCR2-expressing neutrophils from the blood to the pancreatic islets. We further show that pancreatic macrophages secrete IL-1β-inducing CXCR2 ligand production by the β-cells. Finally, the blockade of neutrophil recruitment at early ages using CXCR2 antagonist dampens the diabetogenic T-cell response and the later development of autoimmune diabetes, supporting the therapeutic potential of this approach.
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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.