Research Progress of Mesenchymal Stem Cells in the Treatment of Allergic Rhinitis via the Treg-ILC2 Axis
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摘要: 变应性鼻炎（allergic rhinitis，AR）是由2型炎症驱动的慢性气道疾病，辅助性T细胞（T helper cells，Th）与先天性淋巴样细胞（innate lymphoid cells，ILCs）及其分泌的2型细胞因子是其核心发病机制。近年来，调节性T细胞（regulatory T cells，Tregs）与2组先天性淋巴样细胞（group 2 innate lymphoid cells，ILC2s）之间的免疫失衡（即Treg-ILC2轴）被认为是AR免疫调节的关键环节。间充质干细胞（mesenchymal stem cells，MSCs）凭借其强大的免疫调节潜能，可通过分泌TGF-β、IL-10等可溶性因子，以及基于ICOS-ICOSL（inducible T-cell costimulator-inducible T-cell costimulator ligand）介导的细胞直接接触，有效诱导iTregs分化并抑制ILC2的过度活化。此外，MSC来源的外泌体作为“无细胞疗法”的新策略，展现出更高的安全性和局部递送优势。对Treg与ILC2的交互作用机制进行综述，重点阐述MSCs经Treg-ILC2轴重塑AR免疫平衡的研究进展，旨在为AR的精准免疫靶向治疗提供理论依据与新思路。Abstract: Allergic rhinitis （AR） is a chronic airway disorder predominantly driven by type 2 inflammation, in which T helper （Th） cells, innate lymphoid cells （ILCs）, and their characteristic type 2 cytokines serve as the core pathogenic mechanisms. Recent evidence highlights that the immune imbalance between regulatory T cells （Tregs） and group 2 innate lymphoid cells （ILC2s）, termed as the Treg-ILC2 axis, has been recognized as a critical regulatory hub in AR pathogenesis. Mesenchymal stem cells （MSCs）, characterized by potent immunomodulatory properties, can induce iTreg differentiation and suppress ILC2 hyperactivation through the secretion of soluble factors （e.g., TGF-β, IL-10） and direct cell-to-cell contact mediated by the ICOS-ICOSL （inducible T-cell costimulator-inducible T-cell costimulator ligand ） interaction. By reviewing the cross-talk mechanisms between Tregs and ILC2s, this article focuses on the research progress of MSCs in restoring immune homeostasis in AR via the Treg-ILC2 axis, aiming to provide theoretical foundations and novel insights for precise immune-targeted therapies for AR.
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图 1 变应性鼻炎中 ILC2 驱动 2 型炎症的核心机制及 Treg 调控失衡
Figure 1. Core mechanism of ILC2-driven type 2 inflammation and Treg regulatory imbalance in allergic rhinitis
图 2 间充质干细胞（MSC）经Treg-ILC2轴治疗变应性鼻炎的免疫调节机制
（A） MSCs通过三种主要方式促进Treg细胞的扩增与活化：① 细胞接触依赖机制：MSC表面的ICOSL与Treg表面的ICOS结合，激活PI3K-Akt信号通路；② 旁分泌机制：分泌TGF-β、IL-10、PGE2及IDO等可溶性因子；③ 外泌体机制：释放携带功能性miRNA的细胞外囊泡。（B） 活化后的Treg细胞（iTreg）进而通过两种途径抑制ILC2的功能：① 通过ICOS-ICOSL介导的细胞间接触；② 分泌关键的抑制性细胞因子（IL-10，TGF-β及IL-35）。（C） 最终导致ILC2细胞内核心转录因子GATA3表达下调，2型细胞因子（IL-5，IL-13）分泌减少，从而减轻变应性鼻炎的气道炎症反应。
Figure 2. Immunomodulatory mechanisms of mesenchymal stem cells （MSCs） in the treatment of allergic rhinitis via the Treg-ILC2 axis
表 1 间充质干细胞治疗变应性鼻炎的主要免疫调节机制
Table 1. Principal immunomodulatory mechanisms of mesenchymal stem cells in the treatment of allergic rhinitis
作用方式 关键分子/
信号通路主要免疫调节效应 参考文献 分泌可溶性因子 TGF-β / Smad 信号通路 促进初始 T 细胞向 Tregs 分化；抑制效应 T 细胞增殖；
下调 IL-4、IL-5 表达。[64，65] PGE2 / EP2-EP4 通路 诱导 M1 型巨噬细胞向 M2 型转化；抑制单核细胞向 DCs 分化。 [61][71][76][77] IDO / 犬尿氨酸途径 抑制 Th2 和 Th17 分化；促进 Treg 生成；抑制效应 T 细胞增殖。 [76] 细胞间接触 ICOS - ICOSL 相互作用 激活 PI3K-Akt 通路，直接促进 CD4+ T 细胞向 Tregs 分化，
增强 Treg 对 ILC2 的抑制作用（本文核心机制）。[47][50] PD-L1 / PD-1 结合 阻滞 T 细胞周期于 G0/G1 期，抑制 T 细胞活化与增殖。 [67][68] Notch1 信号通路 调控 T 细胞分化方向，增强 Treg 稳定性。 [68][71] 释放外泌体 miR-146a-5p 靶向 SERPINB2、IRAK1 和 TRAF6，
抑制 ILC2 活化及 Th2 分化。[73][78] miR-125a/b 靶向 STAT3 mRNA 抑制其表达，抑制 Th17 分化。 [68] miR-10 促进 FoxP3 表达，增强 Treg 功能。 [68][79] 
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