ArticleJCI insight2021
Fatty acid binding protein 4 promotes autoimmune diabetes by recruitment and activation of pancreatic islet macrophages.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Targeting the CMKLR1-Mediated Signaling Rebalances Immunometabolism State in Middle-Age Testicular Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The inflammatory path toward type 1 diabetes begins during pregnancy.Nature communications · 2026Article
- Galectin-3 exacerbates autoimmune diabetes by limiting regulatory T cell differentiation and function.Science advances · 2026Article
- Inhibition of fatty acid-binding protein 4 alleviates psoriasis-like skin inflammation by modulating macrophage polarization.Frontiers in immunology · 2026Article
- IL-21 mediates crosstalk between T cells and NK cells during the remission of type 1 diabetes.Nature metabolism · 2026Article
- Metformin Mitigates Diabetes-Driven Renal Senescence via Immunomodulation and the FABP4/FOXO1 Axis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Senescent SPP1Molecular cancer · 2025Article
- Islet Tissue Macrophages in Immunity Homeostasis and Type 1 Diabetes.Clinical reviews in allergy & immunology · 2025Review
- Fatty Acid Binding Protein 4 Regulates the Antigen-Presenting Function of Dendritic Cells Resulting in T Cell Priming in Streptozotocin-Induced Type 1 Diabetes Mice.Journal of diabetes · 2025Article
- FABP7 is increased in progressive multiple sclerosis and induces a pro-inflammatory phenotype in monocytes through a glycolytic switch.Nature communications · 2025Article
- Fabp4 is essential for the maintenance of leukemia stem cells while sparing hematopoietic stem cells.Leukemia · 2025Article
- Assessment of Intestinal Free Fatty Acid Binding Protein 4 in Alopecia Areata Patients.Skin appendage disorders · 2025Article
- Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment?Immune network · 2025Review
- Influences of metabolism and lipid homeostasis on regulatory vs. conventional T cells and implications for autoimmunity.Frontiers in immunology · 2025Review
- Novel FABP4Cell death & disease · 2024Article
- Islet-Resident Memory T Cells Orchestrate the Immunopathogenesis of Type 1 Diabetes through the FABP4-CXCL10 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia-reperfusion injury in steatotic liver transplantation.Cellular and molecular life sciences : CMLS · 2024Article
- Reproductive Profile of Neuronal Androgen Receptor Knockout Female Mice With a Low Dose of DHT.Endocrinology · 2024Article
- IFITM3 promotes glioblastoma stem cell-mediated angiogenesis via regulating JAK/STAT3/bFGF signaling pathway.Cell death & disease · 2024Article
- High-expression of FABP4 in Tubules is a Risk Factor for Poor Prognosis in DKD Patients.Current medicinal chemistry · 2024Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both innate and adaptive immune cells are critical players in autoimmune destruction of insulin-producing β cells in type 1 diabetes. However, the early pathogenic events triggering the recruitment and activation of innate immune cells in islets remain obscure. Here we show that circulating fatty acid binding protein 4 (FABP4) level was significantly elevated in patients with type 1 diabetes and their first-degree relatives and positively correlated with the titers of several islet autoantibodies. In nonobese diabetic (NOD) mice, increased FABP4 expression in islet macrophages started from the neonatal period, well before the occurrence of overt diabetes. Furthermore, the spontaneous development of autoimmune diabetes in NOD mice was markedly reduced by pharmacological inhibition or genetic ablation of FABP4 or adoptive transfer of FABP4-deficient bone marrow cells. Mechanistically, FABP4 activated innate immune responses in islets by enhancing the infiltration and polarization of macrophages to proinflammatory M1 subtype, thus creating an inflammatory milieu required for activation of diabetogenic CD8+ T cells and shift of CD4+ helper T cells toward Th1 subtypes. These findings demonstrate FABP4 as a possible early mediator for β cell autoimmunity by facilitating crosstalk between innate and adaptive immune cells, suggesting that pharmacological inhibition of FABP4 may represent a promising therapeutic strategy for autoimmune diabetes.
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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.