{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T06:37:18Z","timestamp":1788849438704,"version":"build-2803163510"},"reference-count":40,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,7,26]],"date-time":"2025-07-26T00:00:00Z","timestamp":1753488000000},"content-version":"vor","delay-in-days":25,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82200933"],"award-info":[{"award-number":["82200933"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270891"],"award-info":[{"award-number":["82270891"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Diabetes"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Type 1 diabetes is an autoimmune disease with progressive destruction of insulin\u2010producing \u03b2 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Intraperitoneal 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\u2010presenting in dendritic cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that genetic ablation of <jats:italic>FABP4<\/jats:italic> in mice alleviated STZ\u2010induced diabetic damage by reducing diabetogenic T lymphocytes and their production of inflammatory cytokines. In\u00a0vitro studies, <jats:italic>FABP4<\/jats:italic> deficiency dendritic cells expressed lower properties of CD86 and CD80, showing impaired antigen\u2010presenting functions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Genetic ablation of FABP4 in mice alleviated STZ\u2010induced diabetic damage by impairing the antigen\u2010presenting function of dendritic cells through downregulating the phosphorylation levels of the ERK and JNK pathways.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1753-0407.70123","type":"journal-article","created":{"date-parts":[[2025,7,26]],"date-time":"2025-07-26T10:23:45Z","timestamp":1753525425000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Fatty Acid Binding Protein 4 Regulates the Antigen\u2010Presenting Function of Dendritic Cells Resulting\u00a0in T Cell Priming in Streptozotocin\u2010Induced Type\u00a01 Diabetes Mice"],"prefix":"10.1111","volume":"17","author":[{"given":"Hailan","family":"Zou","sequence":"first","affiliation":[{"name":"National Clinical Research Centre for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology The Second Xiangya Hospital of Central South University  Changsha Hunan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingxiang","family":"Xie","sequence":"additional","affiliation":[{"name":"National Clinical Research Centre for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology The Second Xiangya Hospital of Central South University  Changsha Hunan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingyi","family":"Hu","sequence":"additional","affiliation":[{"name":"National Clinical Research Centre for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of 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