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诱导性调节性T细胞在淋巴结中与效应T细胞叠加其抑制能力 抗原特异性S1P1依赖性输出阻断。

Induced Regulatory T Cells Superimpose Their Suppressive Capacity with Effector T Cells in Lymph Nodes Antigen-Specific S1p1-Dependent Egress Blockage.

作者信息

Geng Shuang, Zhong Yiwei, Zhou Xiaoyu, Zhao Gan, Xie Xiaoping, Pei Yechun, Liu Hu, Zhang Huiyuan, Shi Yan, Wang Bin

机构信息

Key Laboratory of Medical Molecular Virology of MOH and MOE, Fudan University Shanghai Medical College, Shanghai, China.

State Key Laboratory for Agro-Biotechnology, China Agricultural University, Beijing, China.

出版信息

Front Immunol. 2017 Jun 7;8:663. doi: 10.3389/fimmu.2017.00663. eCollection 2017.

DOI:10.3389/fimmu.2017.00663
PMID:28638384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5461288/
Abstract

Regulatory T cells (Tregs) restrict overexuberant lymphocyte activation. While close proximity between Tregs and their suppression targets is important for optimal inhibition, and literature indicates that draining lymph nodes (LNs) may serve as a prime location for the suppression, signaling details orchestrating this event are not fully characterized. Using a protocol to enable peripheral generation of inducible antigen-specific Tregs (asTregs) to control allergen-induced asthma, we have identified an antigen-specific mechanism that locks asTregs within hilar LNs which in turn suppresses airway inflammation. The suppressive asTregs, upon antigen stimulation in the LN, downregulate sphingosine-1-phosphate receptor 1 egress receptor expression. These asTregs in turn mediate the downregulation of the same receptor on incoming effector T cells. Therefore, asTregs and effector T cells are locked in these draining LNs for prolonged interactions. Disruption of individual steps of this retention sequence abolishes the inflammation controlled by asTregs. Collectively, this study identifies a new requirement of spatial congregation with their suppression targets essential for asTreg functions and suggests therapeutic programs Treg traffic control.

摘要

调节性T细胞（Tregs）可限制淋巴细胞过度活化。虽然Tregs与其抑制靶标之间的紧密接近对于最佳抑制作用很重要，且文献表明引流淋巴结（LNs）可能是抑制作用的主要部位，但协调这一事件的信号传导细节尚未完全阐明。通过使用一种能够在外周诱导产生可诱导的抗原特异性Tregs（asTregs）以控制变应原诱导的哮喘的方案，我们确定了一种抗原特异性机制，该机制将asTregs锁定在肺门淋巴结内，进而抑制气道炎症。在淋巴结中受到抗原刺激后，具有抑制作用的asTregs会下调鞘氨醇-1-磷酸受体1（S1PR1）这种出胞受体的表达。这些asTregs继而介导传入的效应T细胞上相同受体的下调。因此，asTregs和效应T细胞被锁定在这些引流淋巴结中，以便进行长时间的相互作用。破坏这一滞留序列的各个步骤会消除由asTregs控制的炎症。总体而言，本研究确定了asTregs功能所必需的与抑制靶标进行空间聚集的新要求，并提出了Treg转运控制的治疗方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/7b66bae0f255/fimmu-08-00663-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/5add37c9525e/fimmu-08-00663-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/7b66bae0f255/fimmu-08-00663-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/6e41071eade4/fimmu-08-00663-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/7b59c3656503/fimmu-08-00663-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/9ab44f8907f6/fimmu-08-00663-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0faf/5461288/3eb676d4ee33/fimmu-08-00663-g005.jpg
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