Int J Stomatol ›› 2026, Vol. 53 ›› Issue (1): 36-42.doi: 10.7518/gjkq.2026002

• Stem Cell • Previous Articles     Next Articles

Progress in the study of cellular interactions between dental pulp mesenchymal stem cells and macrophages

Zekai Xu(),Wenzhi Wu,Zhuo Chen()   

  1. Dept. of Conservative and Endodontic Dentistry, Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou 310000, China
  • Received:2024-11-01 Revised:2025-01-15 Online:2026-01-01 Published:2025-12-31
  • Contact: Zhuo Chen E-mail:baixiulinxun@foxmail.com;zoechen@zju.edu.cn
  • Supported by:
    National Natural Science Foundation of China(82270964)

Abstract:

Dental pulp mesenchymal stem cells (or dental pulp stem cells) are mesenchymal stem cells derived from dental pulp tissues, possessing notable capacities for immunomodulation and tissue regeneration. Macrophages, as key immune effector cells, are prevalent in inflammatory microenvironments and exhibit phenotypic plasticity through polarization into distinct functional subsets. Hence, understanding the bidirectional interactions between dental pulp mesenchymal stem cells and macrophages is essential for advancing the therapeutic application of dental pulp mesenchymal stem cells in inflammation-related diseases. This review explores the mechanisms by which dental pulp mesenchymal stem cells influence macrophage polarization, migration, and differentiation and how macrophages of various phenotypes influence the proliferation and differentiation of dental pulp mesenchymal stem cells.

Key words: dental pulp mesenchymal stem cell, macrophage, cellular interaction, immunoregulation, cellular differentiation

CLC Number: 

  • Q25

TrendMD: 

Tab 1

Related studies on the regulatory effect of DPSC on macrophages"

调控作用作用机制实验模型作者年份
增强迁移未探究体外Hu等[4]2021
肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)可上调DPSC中鞘氨醇-1-磷酸(sphingosine-1-phosphate,S1P)的分泌,S1P可增强巨噬细胞向DPSC迁移体外Choi等[5]2022
干扰素-γ(interferon-γ,IFN-γ)可诱导DPSC中单核细胞趋化蛋白-1(monocyte chemoattractant protein,MCP-1)表达,从而增强巨噬细胞向DPSC迁移体外Martinez等[6]2017
脂多糖(lipopolysaccharide,LPS)处理的DPSC可增强巨噬细胞迁移能力,Wnt蛋白生成抑制剂2(inhibitor of Wnt production-2,IWP-2)可消除这一作用体外Chansaenroj等[7]2024
促进M2型极化或(和)抑制M1型极化DPSC可降低LPS处理的巨噬细胞的白细胞介素(interleukin,IL)-6的分泌体外Luo等[3]2022
DPSC可降低LPS处理的巨噬细胞的IL-6和核因子κB(nuclear factor kappa-B,NF-κB)的分泌体外Albashari等[8]2020
DPSC可降低巨噬细胞中TNF-α的表达,增加IL-10和M2型标志物CD206的表达,促进M2型极化体内、体外Omi等[9]2016
DPSC通过分泌转化生长因子-β(transforming growth factor-β,TGF-β)和肝细胞生长因子(hepatocyte growth factor, HGF)并部分失活巨噬细胞丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)通路抑制M1型巨噬细胞体内、体外Li等[10]2021
DPSC可降低脊髓损伤模型中的活性氧(reactive oxygen species,ROS)水平,从而抑制ROS-MAPK-NF-κB P65通路的激活,抑制M1型极化体内、体外Liu等[11]2022
DPSC可通过分泌miRNA-1246,降低巨噬细胞的M1型标志物CD86表达,提高M2型标志物CD206表达体内Shen等[12]2020
DPSC可通过分泌miRNA-125a-3p抑制巨噬细胞Toll样受体(Toll like receptors,TLR)和NF-κB通路,促进M2型极化体外Zheng等[13]2020
DPSC可通过吲哚胺2,3-双加氧酶(indoleamine-2,3-dioxygenase,IDO)抑制LPS处理的巨噬细胞的TNF-α分泌体外Lee等[14]2016
DPSC可通过IDO-犬尿氨酸途径促进M2型极化体外Anderson等[15]2022
DPSC可通过分泌MCP-1促进M2型极化体内、体外Yang等[16]2023
抑制破骨向分化DPSC可通过分泌骨保护素(osteoclastogenesis inhibitory factor,OPG)抑制核因子κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL)/核因子κB受体活化因子(receptor activator of nuclear factor-κB,RANK)通路,抑制巨噬细胞破骨向分化体外Kanji等[17]2021
静脉注射DPSC可降低骨质疏松模型小鼠血清中的RANKL/OPG比例,减少骨丧失体内Kong等[18]2018
相较牙槽骨细胞,DPSC的RANKL表达更低而OPG表达更高,表现出更强的抑制巨噬细胞破骨向分化能力体内Zheng等[19]2015

Fig 1

Cellular interaction between dental pulp mesenchymal stem cells and macrophage"

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