期刊
NATURE MEDICINE
卷 25, 期 7, 页码 1153-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41591-019-0468-5
关键词
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资金
- Open Targets collaboration
- GlaxoSmithKline
- University Medical Center Groningen
- Wellcome [WT206194]
- Lung Foundation Netherlands [5.1.14.020, 4.1.18.226]
- Health-Holland
- Top Sector Life Sciences and Health
- Human Cell Atlas Wellcome Stragetic Science Support [211276/Z/18/Z]
- EMBO
- HFSP
- Marie Curie ENLIGHT-TEN training network
- European Union [753039]
- Helmholtz Association
- German Center for Lung Research (DZL)
- German Research Foundation (DFG) within the Collaborative Research Centre [1243]
- Helmholtz Association [A17, ZT-I-0007]
- Chan Zuckerberg Initiative D.A.F. (advised fund of Silicon Valley Community Foundation) [182835]
- European Research Council [677501 - ZF_Blood]
- Wellcome Trust [211276/Z/18/Z] Funding Source: Wellcome Trust
- Marie Curie Actions (MSCA) [753039] Funding Source: Marie Curie Actions (MSCA)
Human lungs enable efficient gas exchange and form an interface with the environment, which depends on mucosal immunity for protection against infectious agents. Tightly controlled interactions between structural and immune cells are required to maintain lung homeostasis. Here, we use single-cell transcriptomics to chart the cellular landscape of upper and lower airways and lung parenchyma in healthy lungs, and lower airways in asthmatic lungs. We report location-dependent airway epithelial cell states and a novel subset of tissue-resident memory T cells. In the lower airways of patients with asthma, mucous cell hyperplasia is shown to stem from a novel mucous ciliated cell state, as well as goblet cell hyperplasia. We report the presence of pathogenic effector type 2 helper T cells (T(H)2) in asthmatic lungs and find evidence for type 2 cytokines in maintaining the altered epithelial cell states. Unbiased analysis of cell-cell interactions identifies a shift from airway structural cell communication in healthy lungs to a T(H)2-dominated interactome in asthmatic lungs.
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