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中华细胞与干细胞杂志(电子版)

中华细胞与干细胞杂志(电子版) ›› 2025, Vol. 15 ›› Issue (04) : 220 -228. doi: 10.3877/cma.j.issn.2095-1221.2025.04.005

综述

脂肪与骨髓间充质干细胞的免疫调节作用及协同治疗潜力分析
刘沐芸1,2,3, 侯凯翔1,3, 韩奇鹏1,3,6, 崔诗慧1,3, 魏殿华1,3, 符业优1,3, 丁关焱1,3, 从丽萍1,3, 梁晓1,4, 安刚5,†()   
  1. 1518000　深圳科诺医学检验实验室
    2518000　深圳，细胞产业关键共性技术国家工程研究中心
    3518000　深圳芸诺生物科技有限公司
    4518057　深圳市北科生物科技有限公司
    5350000　福州，福建省妇幼保健院细胞医学中心
    6410128　长沙，湖南农业大学动物科学技术学院
  • 收稿日期:2025-02-17 出版日期:2025-08-01
  • 通信作者: 安刚
  • 基金资助:
    细胞产业关键共性技术国家工程研究中心建设项目(发改高技[2023]447号); 深圳市非侵入性细胞质量在线监测和分析平台(F-2022-Z99-502233)

Potential immunomodulatory effects and combined application of adipose-derived mesenchymal stem cells and bone marrow-derived mesenchymal stem cells

Muyun Liu1,2,3, Kaixiang Hou1,3, Qipeng Han1,3,6, Shihui Cui1,3, Dianhua Wei1,3, Yeyou Fu1,3, Guanyan Ding1,3, Liping Cong1,3, Xiao Liang1,4, Gang An5,†()   

  1. 1Shenzhen Kono Laboratory of Medical Laboratory, Shenzhen 518000, China
    2National Engineering Research Center of Key Generic Technologies for Cell Industry, Shenzhen 518000, China
    3Shenzhen Yunnuo Biotechnology Co., LTD., Shenzhen 518000, China
    4Shenzhen Beike Biotechnology Co., LTD., Shenzhen 518057, China
    5Fujian Women and Children's Hospital-Cell Medicine Center, Fuzhou 350000, China
    6College of Animal Science and Tehnology, Hunan Agricultural University, Changsha 410128, China
  • Received:2025-02-17 Published:2025-08-01
  • Corresponding author: Gang An
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引用本文：

刘沐芸, 侯凯翔, 韩奇鹏, 崔诗慧, 魏殿华, 符业优, 丁关焱, 从丽萍, 梁晓, 安刚. 脂肪与骨髓间充质干细胞的免疫调节作用及协同治疗潜力分析[J/OL]. 中华细胞与干细胞杂志(电子版), 2025, 15(04): 220-228.

Muyun Liu, Kaixiang Hou, Qipeng Han, Shihui Cui, Dianhua Wei, Yeyou Fu, Guanyan Ding, Liping Cong, Xiao Liang, Gang An. Potential immunomodulatory effects and combined application of adipose-derived mesenchymal stem cells and bone marrow-derived mesenchymal stem cells[J/OL]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2025, 15(04): 220-228.

脂肪间充质干细胞（ADMSCs）与骨髓间充质干细胞（BMSCs）作为成体干细胞的重要来源，在免疫调节和组织修复领域展现出巨大的潜力。本文系统综述ADMSCs与BMSCs对T细胞（Th1/Th2/Th17/Treg）、B细胞、树突状细胞、巨噬细胞及自然杀伤（NK）细胞的调控机制，揭示二者在免疫抑制途径上的共性与特性。二者通过时空协同效应提升疗效，而异源细胞混合治疗面临生物安全性挑战。本文进一步提出标准化质量控制体系及动态剂量调控策略，为优化干细胞治疗提供理论依据与转化路径。

关键词: 骨髓间充质干细胞, 脂肪间充质干细胞, 免疫调节, 干细胞治疗

Adipose-derived mesenchymal stem cells (ADMSCs) and bone marrow-derived mesenchymal stem cells (BMSCs), as crucial sources of adult stem cells, exhibiting significant potential in the fields of immunomodulation and tissue repair. This article systematically reviews the regulatory mechanisms of ADMSCs and BMSCs on T cells (Th1/Th2/Th17/Treg), B cells, dendritic cells, macrophages, and natural killer (NK) cells, elucidating their shared and distinct characteristics in immunosuppressive pathways. Their spatiotemporal synergistic effects significantly enhance therapeutic efficacy, while heterologous cell combination therapy faces biosafety challenges. Furthermore, this study proposes a standardized quality control system and dynamic dosage regulation strategy, providing a theoretical foundation and translational pathway for optimizing stem cell therapy.

Key words: Bone marrow-derived mesenchymal stem cells, Adipose-derived mesenchymal stem cells, Immunomodulation, Stem cell therapy
表1 BMSCs免疫调节作用机制与功能效应
免疫细胞类型 作用机制 涉及的因子/分子 功能效果
CD4+ T细胞 直接抑制增殖：抑制IL-2分泌及自然杀伤细胞活性；上调CD4+ CD25+ Treg细胞，抑制IFN-γ、IL-4等促炎因子[13]；在炎症环境中促进IL-17产生[11] TGF-β、Foxp3、IL-2、IFN-γ、IL-4、IL-17[9] 抑制T细胞活化[10]和炎症反应[9]，促进免疫耐受
Th1/Th2细胞 降低IL-17、IL-22、IFN-γ、TNF-α水平；抑制CD4+ T细胞向Th1分化；增加Th2细胞数量，改变Th1/Th2比例；通过CCR6抑制Th1细胞黏附[9] IL-17、IL-22、IFN-γ、TNF-α、CCR6[9] 抑制促炎反应，增强抗炎作用，促进Treg细胞功能[9]
Treg TGF-β促进Fox3表达，增强Treg扩增[11]；通过分泌可溶性因子增强Treg的抗炎作用[11] TGF-β、Foxp3、IL-10[11] 增强免疫抑制和抗炎功能[11]
CD8+ T细胞 直接接触抑制：通过BMSCs表面MICA/B与CD8+ T细胞NKG2D结合，下调NKG2D表达；分泌PGE2、IDO、TGF-β抑制活性[10] MICA/B、NKG2D、PGE2、IDO、TGF-β[14] 抑制增殖和细胞毒性功能[14]
B细胞 直接抑制B细胞增殖[11] 未明确具体因子 抑制B细胞活化和抗体产生[11]
DCs 抑制IL-1等细胞因子，减少促炎因子（IFN-γ、IL-12、TNF-α）分泌；促进抗炎因子IL-10分泌[11,15] IL-1、IFN-γ、IL-12、TNF-α、IL-10[11,15] 降低DCs对T细胞的刺激能力，抑制炎症反应[15]
巨噬细胞/小胶质细胞 促进M1型（促炎）向M2型（抗炎）转化[16]；减少TNF-α、IL-1β分泌，增加IL-10、TGF-β分泌[17]；通过调节AMPK/NF-κB通路抑制活化[18]；分泌TSG-6抑制TLR2/MyD88/NF-κB通路[18] TNF-α、IL-1β、IL-10、TGF-β、AMPK/NF-κB、TSG-6[16,17,18] 减轻神经炎症和中枢敏化[18]，缓解疼痛，抑制过度免疫反应[16]
NK细胞 抑制静息态NK细胞增殖和IFN-γ分泌（通过IDO、PGE2）[19]；增强IL-12/IL-18预激活NK细胞的IFN-γ分泌（保留细胞毒性功能）[19]；抑制IL-12/IL-18诱导的NK细胞活性[19] IDO、PGE2、IL-12、IL-18、IFN-γ[19,20] 双向调节：抑制静息态NK细胞功能，增强激活态NK细胞的抗病毒、肿瘤反应能力[19]
表2 ADMSCs免疫调节作用机制与功能效应
免疫细胞类型 作用机制 涉及的因子/分子 功能效果
T细胞 抑制T细胞增殖与活化；诱导T细胞凋亡或失能 TGF-β、IL-10、PGE2、IDO[21,23] 减少T细胞过度活化，维持免疫耐受[21]
Th1细胞 抑制Th1分化与功能[24]；下调Th1相关转录因子[25] IDO（降解色氨酸）、TGF-β、STAT1/4抑制、T-bet下调[24,25] 降低IFN-γ和TNF-α分泌，减轻Th1介导的炎症[24,25]
Th2细胞 调节Th1/Th2平衡，可能增强Th2反应（微环境依赖性）[26] 上调GATA-3[33]，IL-4/IL-5/IL-13分泌增加（间接调控） 抑制Th1/Th17主导的炎症，但可能加重Th2相关过敏性疾病[26]
Th17细胞 抑制Th17分化与IL-17A分泌；阻断IL-23信号通路 IL-10、TGF-β、IL-6/IL-23受体抑制、RORγt下调[28,29] 减少Th17介导的自身免疫损伤[28,29]
Treg 促进Treg扩增与功能活化[30]；抑制Treg向Th17转化[32] IDO、TGF-β、IL-10、Foxp3上调[34] 增强免疫抑制功能，缓解GVHD和自身免疫病[31]
B细胞 抑制B细胞增殖与抗体产生；调节浆细胞分化[35] 分泌IL-10和TGF-β[35] 减少T细胞激活，促进免疫耐受[35]
DCs 抑制树突细胞成熟与抗原呈递功能[36] 分泌IL-10和PGE2，减少CD80和CD86表达[36,37] 减轻炎症反应并维持免疫耐受[37]
巨噬细胞/小胶质细胞 促炎M1型向抗炎M2型极化[38,30] 分泌抗炎因子IL-10和TGF-β，激活巨噬细胞中的STAT3信号通路[38] 减轻组织炎症，促进修复[39]
表3 BMSCs和ADMSCs对免疫细胞亚群的差异化调控
免疫细胞类型 BMSCs作用特征 ADMSCs作用特征
T细胞 （1）抑制CD4+/CD8+ T增殖（非MHC限制性）；（2）通过TGF-β增强Treg功能[51] （1）优先抑制Th1/Th17分化；（2）通过IDO促进Treg扩增[52]
巨噬细胞 促进M1→M2极化（PI3K/AKT通路激活）[53] 间接调控M2极化（文献未明确通路）[53]
NK细胞 双向调节：抑制静息态NK活性，增强IL-12/IL-18激活的NK功能 未明确直接作用[54]
DCs 抑制IL-12分泌，降低T细胞活化能力[55] 诱导耐受性DCs生成[56]
表4 BMSCs和ADMSCs的分子通路与关键调控因子对比
通路/因子 BMSCs主要关联 ADMSCs主要关联
免疫抑制通路 TGF-β/Smad、IDO-Kynurenine、PGE2-EP2/EP4[57] IDO-T-bet抑制、IL-23R-STAT3阻断[58]
促修复通路 PI3K/AKT （抗凋亡）、TSG-6- TLR2/ MyD88 （抗炎）[58] GATA-3介导的Th2极化、Foxp3-Treg扩增[59]
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