调节性T细胞基础机制研究突破和临床转化前景

doi:10.3969/j.issn.1674-8115.2026.04.001

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (4): 415-426.doi: 10.3969/j.issn.1674-8115.2026.04.001

• 前沿述评 •

调节性T细胞基础机制研究突破和临床转化前景

王震¹, 张楠¹, 沈艺冰², 李丹², 彭程¹(), 顾志冬³^,⁴^,⁵(), 李斌¹^,²^,³()

^1.上海交通大学医学院海南国际医学中心临床免疫与治疗实验室，琼海 571400
^2.上海交通大学医学院免疫学与微生物学系，上海市免疫学研究所免疫相关疾病研究中心，上海 200025
^3.上海交通大学海南研究院，三亚 572025
^4.上海交通大学医学院附属瑞金医院，上海 200025
^5.上海交通大学医学院附属瑞金医院海南医院（海南博鳌研究型医院），琼海 571400

收稿日期:2025-12-02 接受日期:2026-01-21 出版日期:2026-04-17 发布日期:2026-04-17
通讯作者: 李斌，教授，博士；电子信箱：binli@shsmu.edu.cn
顾志冬，教授，博士；电子信箱：13806153534@163.com
彭程，工程师，博士；电子信箱：chpeng2005@163.com。
作者简介:第一联系人：为共同第一作者（co-first authors）。
基金资助:
国家自然科学基金(82441047);国家自然科学基金(82241222);国家自然科学基金(32130041);国家科技重大专项(2023ZD0501605)

Breakthroughs in basic mechanism research and clinical translation prospects of regulatory T cells

Wang Zhen¹, Zhang Nan¹, Shen Yibing², Li Dan², Peng Cheng¹(), Gu Zhidong³^,⁴^,⁵(), Li Bin¹^,²^,³()

^1.Clinical Immunology and Therapy Laboratory, Hainan International Medical Center, Shanghai Jiao Tong University School of Medicine, Qionghai 571400, China
^2.Center for Immune-Related Diseases at Shanghai Institute of Immunology; Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
^3.Shanghai Jiao Tong University Hainan Research Institute, Sanya 572025, China
^4.Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
^5.Hainan Branch, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine (Hainan Boao Research Hospital), Qionghai 571400, China

Received:2025-12-02 Accepted:2026-01-21 Online:2026-04-17 Published:2026-04-17
Contact: Li Bin, E-mail: binli@shsmu.edu.cn
Gu Zhidong, E-mail: 13806153534@163.com
Peng Cheng, E-mail: chpeng2005@163.com.
Supported by:
National Natural Science Foundation of China(82441047);National Science and Technology Major Project(2023ZD0501605)

摘要/Abstract

摘要：

免疫耐受是维持机体免疫系统稳态的核心基石，一旦这一精密调控机制发生紊乱，将直接诱发类风湿关节炎、系统性红斑狼疮等自身免疫病，以及肿瘤细胞免疫逃逸、器官移植排斥等一系列表现，严重威胁人类生命健康。2025年诺贝尔生理学/医学奖被授予玛丽·E·布伦科（Mary E. Brunkow）、弗雷德·拉姆斯德尔（Fred Ramsdell）与坂口志文（Shimon Sakaguchi），以表彰他们在外周免疫耐受领域的开创性贡献——成功鉴定CD4⁺CD25⁺FOXP3⁺调节性T细胞（regulatory T cell，T_reg）及其核心调控基因——叉头框蛋白P3（forkhead box P3，FOXP3），建立了“FOXP3-T_reg-免疫耐受”的核心理论框架，为后续相关研究的开展奠定了坚实基础。该综述系统梳理T_reg与FOXP3研究的历史脉络，从早期对免疫耐受现象的初步探索，到关键细胞亚群与调控基因的鉴定，清晰呈现领域发展的演进历程；重点聚焦近年来的关键进展，全面涵盖T_reg亚型的精细分类与发育特征、FOXP3调控网络的多维度拓展、T_reg在多种疾病中的功能机制解析及临床转化的突破性成果等核心内容，最后围绕T_reg疗法的临床转化瓶颈对未来发展方向进行展望。

关键词: 调节性T细胞, 叉头框蛋白P3, 免疫耐受, 免疫稳态, 临床转化

Abstract:

Immune tolerance serves as the core cornerstone for maintaining the homeostasis of the body's immune system. Once this sophisticated regulatory mechanism is disrupted, it will directly induce a series of major diseases, including autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus, as well as tumor immune escape and organ transplant rejection, seriously endangering human life and health. The 2025 Nobel Prize in Physiology or Medicine was awarded to Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi in recognition of their pioneering contributions to the field of peripheral immune tolerance—successfully identifying CD4⁺CD25⁺FOXP3⁺ regulatory T cells (T_reg) and their core regulatory gene, forkhead box P3 (FOXP3), and establishing the core theoretical framework of the “FOXP3-T_reg-immune tolerance” axis, which has laid a solid foundation for subsequent research in this field. This review systematically combs the historical context of T_reg and FOXP3 research, clearly presenting the evolutionary trajectory of the field from the early exploration of immune tolerance phenomena to the identification of key cell subsets and regulatory genes. It focuses on key advances in recent years, comprehensively covering core contents such as the refined classification and developmental characteristics of T_reg subtypes, the multi-dimensional expansion of the FOXP3 regulatory network, the functional mechanisms of T_reg in various diseases, and breakthrough achievements in clinical translation. Finally, focusing on the bottlenecks in the clinical translation of T_reg therapies, this review provides perspectives on future development directions.

Key words: regulatory T cell (T_reg), forkhead box P3 (FOXP3), immune tolerance, immune homeostasis, clinical translation

中图分类号:

R392.12

王震, 张楠, 沈艺冰, 李丹, 彭程, 顾志冬, 李斌. 调节性T细胞基础机制研究突破和临床转化前景[J]. 上海交通大学学报（医学版）, 2026, 46(4): 415-426.

Wang Zhen, Zhang Nan, Shen Yibing, Li Dan, Peng Cheng, Gu Zhidong, Li Bin. Breakthroughs in basic mechanism research and clinical translation prospects of regulatory T cells[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(4): 415-426.

图/表 2

图1 Treg 亚型和发育特征Note： This figure illustrates the subclassification of Treg and associated molecular mechanisms, including tTreg, pTreg, and iTreg. tTreg develop in the thymus under T cell receptor (TCR) and IL-2 signaling, with stable FOXP3 expression maintained by demethylation of conserved non-coding sequence 2 (CNS2). pTreg arise from naive T cells in peripheral tissues in response to transforming growth factor-β (TGF-β), antigen, and short-chain fatty acids (SCFAs), leading to transient FOXP3 expression. iTreg are generated using IL-2 and TGF-β, but exhibit unstable FOXP3 expression due to CNS2 methylation. The distinct epigenetic and environmental cues shape Treg stability and functions across different developmental pathways. TSDR—Treg-specific demethylated region; CLA—cutaneous lymphocyte-associated antigen; CCR4—C-C chemokine receptor 4; RORγt—RAR-related orphan receptor γt.

Fig 1 Subtypes and developmental characteristics of Treg

图2 Treg 多重免疫抑制机制Note： This diagram illustrates the key immunosuppressive mechanisms of Treg. Treg exert immunosuppressive effects through multiple synergistic pathways, with specific mechanisms as follows: ①CTLA-4 expressed on the surface of Treg can bind to co-stimulatory molecules CD80/CD86 on antigen-presenting cells (APCs), competitively inhibiting CD28-mediated co-stimulatory signaling in T cells, while inducing APCs to express indoleamine 2,3-dioxygenase (IDO), thereby inhibiting T cell proliferation via metabolic pathways. ②Treg highly express IL-2R, which enables them to efficiently sequester IL-2 in the microenvironment, reducing the availability of this key cytokine required for conventional T cell (Tcon) activation, and thereby inhibiting the proliferation and functional exertion of Tcon. ③Treg can secrete multiple anti-inflammatory cytokines, such as IL-10, IL-35, and TGF-β, which suppress immune responses. ④CD39 and CD73 expressed on the surface of Treg can hydrolyze ATP in the microenvironment to generate adenosine; upon binding to the A2A adenosine receptor (A2AR) on Tcon, adenosine inhibit the activity of Tcon. ⑤Treg can induce apoptosis of Tcon by secreting granzyme and perforin.

Fig 2 Multilayered immunosuppressive mechanisms of Treg

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调节性T细胞基础机制研究突破和临床转化前景

Breakthroughs in basic mechanism research and clinical translation prospects of regulatory T cells

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