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皮肤引流淋巴结中CCR10(+)固有淋巴细胞的选择性编程对皮肤稳态调节的作用

Selective programming of CCR10(+) innate lymphoid cells in skin-draining lymph nodes for cutaneous homeostatic regulation.

作者信息

Yang Jie, Hu Shaomin, Zhao Luming, Kaplan Daniel H, Perdew Gary H, Xiong Na

机构信息

Center for Molecular Immunology and Infectious Disease, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA.

Department of Dermatology, Center for Immunology, University of Minnesota, Minneapolis, Minnesota, USA.

出版信息

Nat Immunol. 2016 Jan;17(1):48-56. doi: 10.1038/ni.3312. Epub 2015 Nov 2.

DOI:10.1038/ni.3312
PMID:26523865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4838393/
Abstract

Innate lymphoid cells (ILCs) 'preferentially' localize into barrier tissues, where they function in tissue protection but can also contribute to inflammatory diseases. The mechanisms that regulate the establishment of ILCs in barrier tissues are poorly understood. Here we found that under steady-state conditions, ILCs in skin-draining lymph nodes (sLNs) were continuously activated to acquire regulatory properties and high expression of the chemokine receptor CCR10 for localization into the skin. CCR10(+) ILCs promoted the homeostasis of skin-resident T cells and, reciprocally, their establishment in the skin required T cell-regulated homeostatic environments. CD207(+) dendritic cells expressing the transcription factor Foxn1 were required for the proper generation of CCR10(+) ILCs. These observations reveal mechanisms that underlie the specific programming and priming of skin-homing CCR10(+) ILCs in the sLNs.

摘要

固有淋巴细胞(ILCs)“优先”定位于屏障组织,在那里它们发挥组织保护作用,但也可能导致炎症性疾病。调节ILCs在屏障组织中建立的机制尚不清楚。在这里,我们发现,在稳态条件下,皮肤引流淋巴结(sLNs)中的ILCs持续被激活,以获得调节特性和趋化因子受体CCR10的高表达,从而定位于皮肤。CCR10(+) ILCs促进皮肤驻留T细胞的稳态,相反,它们在皮肤中的建立需要T细胞调节的稳态环境。表达转录因子Foxn1的CD207(+)树突状细胞是正确生成CCR10(+) ILCs所必需的。这些观察结果揭示了sLNs中皮肤归巢CCR10(+) ILCs的特定编程和启动的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/00c6040ad1c4/nihms727230f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/86654f05e68f/nihms727230f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/3eeb2f5e16da/nihms727230f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/59dfb772bce2/nihms727230f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/00dfe50c5a02/nihms727230f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/0fc8da5a42f0/nihms727230f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/00c6040ad1c4/nihms727230f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/86654f05e68f/nihms727230f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/3eeb2f5e16da/nihms727230f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/59dfb772bce2/nihms727230f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/00dfe50c5a02/nihms727230f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/0fc8da5a42f0/nihms727230f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a716/4838393/00c6040ad1c4/nihms727230f6.jpg

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