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体内调节性T细胞对树突状细胞的II类主要组织相容性复合体非依赖性抑制性黏附作用

Class II MHC-independent suppressive adhesion of dendritic cells by regulatory T cells in vivo.

作者信息

Yan Jiacong, Liu Bo, Shi Yan, Qi Hai

机构信息

Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing 10084, China.

School of Life Sciences, Tsinghua University, Beijing 10084, China.

出版信息

J Exp Med. 2017 Feb;214(2):319-326. doi: 10.1084/jem.20160629. Epub 2017 Jan 12.

DOI:10.1084/jem.20160629
PMID:28082359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5294853/
Abstract

Regulatory T (T reg) cells are essential for peripheral homeostasis and known to target and suppress dendritic cells (DCs). One important mechanism is through prolonged interaction between antigen-specific T reg cells and DCs that down-regulates the co-stimulatory capacity of DCs. However, the dynamics and TCR specificities of such T reg cell-DC interaction and its relevance to the suppressive outcomes for individual DCs have not been clarified. To gain insights into the underlying cellular events in vivo, we analyzed individual T reg cell-DC interaction events in lymph nodes by intravital microscopy. Our results show that, upon exposure to interleukin-2, T reg cells formed prolonged adhesive contact with DCs, independent of antigen or MHC recognition, which significantly suppressed the contemporaneous interaction of the same DCs with antigen-specific conventional T cells and impaired T cell priming. Therefore, T reg cells may function in part as feedback regulators in inflammatory milieu, by suppressing local DCs and interrupting immune activation in a contact-dependent and class II MHC-independent manner.

摘要

调节性T（Treg）细胞对于外周稳态至关重要，已知其可靶向并抑制树突状细胞（DC）。一种重要机制是通过抗原特异性Treg细胞与DC之间的长时间相互作用，从而下调DC的共刺激能力。然而，这种Treg细胞与DC相互作用的动力学和TCR特异性及其与单个DC抑制结果的相关性尚未阐明。为了深入了解体内潜在的细胞事件，我们通过活体显微镜分析了淋巴结中单个Treg细胞与DC的相互作用事件。我们的结果表明，在暴露于白细胞介素-2后，Treg细胞与DC形成了长时间的粘附接触，这与抗原或MHC识别无关，显著抑制了同一DC与抗原特异性常规T细胞的同时相互作用，并损害了T细胞启动。因此，Treg细胞可能部分作为炎症环境中的反馈调节因子，通过以接触依赖和II类MHC非依赖的方式抑制局部DC并中断免疫激活来发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/dfcb5e2c47a0/JEM_20160629_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/e20b80d8ef5d/JEM_20160629_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/cac09d92cbfb/JEM_20160629_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/dc0f39204cf4/JEM_20160629_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/dfcb5e2c47a0/JEM_20160629_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/e20b80d8ef5d/JEM_20160629_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/cac09d92cbfb/JEM_20160629_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/dc0f39204cf4/JEM_20160629_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7f/5294853/dfcb5e2c47a0/JEM_20160629_Fig4.jpg

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