ArticleJournal of diabetes2025
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.
Article in Journal of diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes.Poultry science · 2026Article
- FABP4 as an immunometabolic hub in preeclampsia: from maternal-fetal interface to systemic inflammation.Frontiers in immunology · 2026Review
- 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
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Authors and funding
9 authors.
Funding
Abstract
backgroundType 1 diabetes is an autoimmune disease with progressive destruction of insulin-producing β cells in islets of Langerhans of the pancreas. However, the early pathogenic factors triggering the recruitment and activation of innate immune cells remain unclear. A study reported that FABP4 accelerates the onset of type 1 diabetes in NOD mice by inducing the polarization of proinflammatory macrophages and their infiltration into pancreatic islets. Nonetheless, the role of FABP4 in mediating crosstalk between innate immunity and adaptive immunity in T1D is unclear.
methodsIntraperitoneal injections of streptozotocin were used to establish a type 1 diabetes mouse model. Blood glucose was monitored, and intraperitoneal glucose tolerance test (IPGTT) was conducted to compare glucose homeostasis. The peripheral immune cells were detected using flow cytometry. Mixed lymphocyte reactions were applied to examine the function of FABP4 on antigen-presenting in dendritic cells.
resultsWe found that genetic ablation of FABP4 in mice alleviated STZ-induced diabetic damage by reducing diabetogenic T lymphocytes and their production of inflammatory cytokines. In vitro studies, FABP4 deficiency dendritic cells expressed lower properties of CD86 and CD80, showing impaired antigen-presenting functions.
conclusionsGenetic ablation of FABP4 in mice alleviated STZ-induced diabetic damage by impairing the antigen-presenting function of dendritic cells through downregulating the phosphorylation levels of the ERK and JNK pathways.
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