文献类型：期刊文献

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

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

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]East China Univ Sci & Technol, Engn Res Ctr Biomed Mat, Minist Educ, Shanghai 200237, Peoples R China;[3]East China Univ Sci & Technol, Key Lab Ultrafine Mat, Minist Educ, Shanghai 200237, Peoples R China;[4]East China Univ Sci & Technol, Frontiers Sci Ctr Materiobiol & Dynam Chem, Shanghai 200237, Peoples R China

年份：2026

卷号：55

起止页码：640

外文期刊名：BIOACTIVE MATERIALS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001598504900001)】；

基金：This work was 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) . The authors thank the staff members of the Integrated Laser Microscopy System at the National Facility for Protein Science in Shanghai (NFPS) , Shanghai Advanced Research Institute, Chinese Academy of Sciences, Zhangjiang Lab, China for sample preparation, data collection and analysis.

语种：英文

外文关键词：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-PPAR gamma cascade, 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.