文献类型：期刊文献

中文题名：Sulfated polysaccharide facilitates macrophage-Treg crosstalk to mitigate chronic inflammation in diabetic wound healing

作者：Tong Shen[1,2];Hao Xu[1,2];Kai Dai[2,3,4];Jing Wang[1,2,3];Changsheng Liu[2,3,4]

机构：[1]State Key Laboratory of Bioreactor Engineering,East China University of Science and Technology,Shanghai,200237,PR China;[2]Engineering Research Center for Biomedical Materials of the Ministry of Education,East China University of Science and Technology,Shanghai,200237,PR China;[3]Key Laboratory for Ultrafine Materials of the Ministry of Education,East China University of Science and Technology,Shanghai,200237,PR China;[4]Frontiers Science Center for Materiobiology and Dynamic Chemistry,East China University of Science and Technology,Shanghai,200237,PR China

年份：2026

卷号：55

期号：1

起止页码：640

中文期刊名：Bioactive Materials

外文期刊名：生物活性材料(英文)

基金：supported by the Key Program of the National Natural Science Foundation of China(no.32230059);the Basic Science Center Program(no.T2288102);the National Natural Science Foundation of China(32301123);the Foundation of Frontiers Science Center for Materiobiology and Dynamic Chemistry(no.JKVD1211002).

语种：英文

中文关键词：Diabetic wound healing;Regulatory T cells;Immune;Microneedles;Macrophages

摘要：Diabetic wounds struggle to heal due to chronic inflammation and immune dysregulation,in which regulatory T cells(Tregs)are critical for inflammation resolution and tissue repair.However,effective strategies for ondemand Treg recruitment remain elusive.Here,we innovatively integrated sulfated chitosan(SCS)-a chemically modified polysaccharide-with a microneedle structure to engineer an active immunomodulatory delivery system.The engineered sulfation domains confer synergistic cytokine-binding capacity to SCS,thereby equipping the material with enhanced functionality in immunomodulation.Mechanistically,SCS drives macrophage polarization via the IL-4/STAT6-PPARγcascade,triggering CCL22-dependent Treg chemotaxis.The SCS establishes bidirectional macrophage-Treg crosstalk,enabling self-sustaining inflammation resolution through M2 phenotype stabilization and Treg-mediated feedback loops.This biomaterial-driven coordination between innate and adaptive immunity surpasses passive drug delivery approaches,effectively reducing inflammation and promoting wound healing without the need for exogenous biologics.Our work pioneers endogenous immunity harnessing through biomaterial design,offering a paradigm shift for diabetic wound therapeutics.