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自噬通过将环境线索与代谢稳态相结合来维持调节性T细胞的功能完整性。

Autophagy enforces functional integrity of regulatory T cells by coupling environmental cues and metabolic homeostasis.

作者信息

Wei Jun, Long Lingyun, Yang Kai, Guy Cliff, Shrestha Sharad, Chen Zuojia, Wu Chuan, Vogel Peter, Neale Geoffrey, Green Douglas R, Chi Hongbo

机构信息

Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Nat Immunol. 2016 Mar;17(3):277-85. doi: 10.1038/ni.3365. Epub 2016 Jan 25.

DOI:10.1038/ni.3365
PMID:26808230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4755832/
Abstract

Regulatory T (Treg) cells respond to immune and inflammatory signals to mediate immunosuppression, but how the functional integrity of Treg cells is maintained under activating environments is unclear. Here we show that autophagy is active in Treg cells and supports their lineage stability and survival fitness. Treg cell-specific deletion of Atg7 or Atg5, two essential genes in autophagy, leads to loss of Treg cells, greater tumor resistance and development of inflammatory disorders. Atg7-deficient Treg cells show increased apoptosis and readily lose expression of the transcription factor Foxp3, especially after activation. Mechanistically, autophagy deficiency upregulates metabolic regulators mTORC1 and c-Myc and glycolysis, which contribute to defective Treg function. Therefore, autophagy couples environmental signals and metabolic homeostasis to protect lineage and survival integrity of Treg cells in activating contexts.

摘要

调节性T（Treg）细胞对免疫和炎症信号作出反应以介导免疫抑制，但在激活环境下Treg细胞的功能完整性是如何维持的尚不清楚。在此我们表明，自噬在Treg细胞中活跃，并支持其谱系稳定性和生存适应性。自噬的两个关键基因Atg7或Atg5在Treg细胞中的特异性缺失会导致Treg细胞丧失、更强的肿瘤抗性以及炎症性疾病的发展。Atg7缺陷的Treg细胞显示出凋亡增加，并容易丧失转录因子Foxp3的表达，尤其是在激活后。从机制上讲，自噬缺陷会上调代谢调节因子mTORC1和c-Myc以及糖酵解，这导致Treg功能缺陷。因此，自噬将环境信号与代谢稳态联系起来，以在激活环境中保护Treg细胞的谱系和生存完整性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/af7295373071/nihms742544f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/ad657cc1aa35/nihms742544f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/58f7ec66fec0/nihms742544f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/17a6a5e3ceaa/nihms742544f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/8b33c3fd78de/nihms742544f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/faf6035267af/nihms742544f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/a716a11c101b/nihms742544f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/af7295373071/nihms742544f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/ad657cc1aa35/nihms742544f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/58f7ec66fec0/nihms742544f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/17a6a5e3ceaa/nihms742544f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/8b33c3fd78de/nihms742544f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/faf6035267af/nihms742544f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/a716a11c101b/nihms742544f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cc8/4755832/af7295373071/nihms742544f7.jpg

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[3]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

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Nat Immunol. 2015-11

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Nat Immunol. 2015-2

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Nat Immunol. 2015-2

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Nat Immunol. 2014-4-13

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