| Literature DB >> 31209336 |
Felipe A Vieira Braga1,2, Gozde Kar1,2, Marijn Berg3,4, Orestes A Carpaij4,5, Krzysztof Polanski1, Lukas M Simon6, Sharon Brouwer3,4, Tomás Gomes1, Laura Hesse3,4, Jian Jiang3,4, Eirini S Fasouli1,2, Mirjana Efremova1, Roser Vento-Tormo1, Carlos Talavera-López1, Marnix R Jonker3,4, Karen Affleck7, Subarna Palit6,8,9,10, Paulina M Strzelecka1,11,12, Helen V Firth1, Krishnaa T Mahbubani13, Ana Cvejic1,11,12, Kerstin B Meyer1, Kourosh Saeb-Parsy13, Marjan Luinge3,4, Corry-Anke Brandsma3,4, Wim Timens3,4, Ilias Angelidis14, Maximilian Strunz14, Gerard H Koppelman4,15, Antoon J van Oosterhout7, Herbert B Schiller14, Fabian J Theis6,16, Maarten van den Berge4,5, Martijn C Nawijn17,18, Sarah A Teichmann19,20,21.
Abstract
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 (TH2) 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 TH2-dominated interactome in asthmatic lungs.Entities:
Mesh：
Year: 2019 PMID： 31209336 DOI： 10.1038/s41591-019-0468-5
Source DB: PubMed Journal: Nat Med ISSN： 1078-8956 Impact factor: 53.440