Author: Christoph Muus; Malte D Luecken; Gokcen Eraslan; Avinash Waghray; Graham Heimberg; Lisa Sikkema; Yoshihiko Kobayashi; Eeshit Dhaval Vaishnav; Ayshwarya Subramanian; Christopher Smillie; Karthik Jagadeesh; Elizabeth Thu Duong; Evgenij Fiskin; Elena Torlai Triglia; Christophe Becavin; Meshal Ansari; Peiwen Cai; Brian Lin; Justin Buchanan; Sijia Chen; Jian Shu; Adam L Haber; Hattie Chung; Daniel T Montoro; Taylor Adams; Hananeh Aliee; Samuel J Allon; Zaneta Andrusivova; Ilias Angelidis; Orr Ashenberg; Kevin Bassler; Christophe Becavin; Inbal Benhar; Joseph Bergenstrahle; Ludvig Bergenstrahle; Liam Bolt; Emelie Braun; Linh T Bui; Mark Chaffin; Evgeny Chichelnitskiy; Joshua Chiou; Thomas M Conlon; Michael S Cuoco; Marie Deprez; David S Fischer; Astrid Gillich; Joshua Gould; Minzhe Guo; Austin J Gutierrez; Arun C Habermann; Tyler Harvey; Peng He; Xiaomeng Hou; Lijuan Hu; Alok Jaiswal; Peiyong Jiang; Theodoros Kapellos; Christin S Kuo; Ludvig Larsson; Michael A Leney-Greene; Kyungtae Lim; Monika Litvinukova; Ji Lu; Leif S Ludwig; Wendy Luo; Henrike Maatz; Elo Maddissoon; Lira Mamanova; Kasidet Manakongtreecheep; Charles-Hugo Marquette; Ian Mbano; Alexi M McAdams; Ross J Metzger; Ahmad N Nabhan; Sarah K Nyquist; Jose Ordovas-Montanes; Lolita Penland; Olivier B Poirion; Segio Poli; CanCan Qi; Daniel Reichart; Ivan Rosas; Jonas Schupp; Rahul Sinha; Rene V Sit; Kamil Slowikowski; Michal Slyper; Neal Smith; Alex Sountoulidis; Maximilian Strunz; Dawei Sun; Carlos Talavera-Lopez; Peng Tan; Jessica Tantivit; Kyle J Travaglini; Nathan R Tucker; Katherine Vernon; Marc H Wadsworth; Julia Waldman; Xiuting Wang; Wenjun Yan; Ali Onder Yildirim; William Zhao; Carly G K Ziegler; Aviv Regev
Title: Integrated analyses of single-cell atlases reveal age, gender, and smoking status associations with cell type-specific expression of mediators of SARS-CoV-2 viral entry and highlights inflammatory programs in putative target cells Document date: 2020_4_20
ID: nkql7h9x_29
Snippet: The cell programs (Fig. 4c, Extended Data Fig. 11a ,b, Supplementary Table 6 ) were enriched in many of the same genes and pathways as tissue-specific programs (Fig. 4d , Supplementary Table 6 ,7,8,9,10), and highlight a potential role for TNF signaling in ACE2 regulation. We first confirmed that the cell programs were not merely associated with the number of transcripts per cell (Extended Data Fig. 11c) . While some genes were shared between the.....
Document: The cell programs (Fig. 4c, Extended Data Fig. 11a ,b, Supplementary Table 6 ) were enriched in many of the same genes and pathways as tissue-specific programs (Fig. 4d , Supplementary Table 6 ,7,8,9,10), and highlight a potential role for TNF signaling in ACE2 regulation. We first confirmed that the cell programs were not merely associated with the number of transcripts per cell (Extended Data Fig. 11c) . While some genes were shared between the tissue and cell programs (e.g., many virus-related genes, such as CEACAM5, CXCL17, SLPI, and HLA-DRA), the cell programs further captured unique biological functions and activities. For example, dual positive lung secretory cells differentially expressed genes involved in TNF signaling including RIPK3, a key regulator of inflammatory cell death via necroptosis, previously implicated in SARS-CoV pathogenesis 84 . Both lung dual positive secretory and multiciliated cells differentially expressed lysosomal genes (MFSD8, CTSS, CTNS, CTSH), potentially relevant for endolysosomal entry of coronaviruses 85 . Dual positive AT1 cell programs included genes involved in immunoproteasome (PSMB8, PSMB9, Fig. 4c) , class I and II antigen presentation (HLA-DMA, HLA-DRB5, HLA-DPB1, HLA-DRA, HLA-DPA1), and phagocytosis. Dual-positive nasal goblet cells differentially expressed several cytokines and chemokines, including granulocyte-colony stimulating factor (CSF3), which may impact hematopoiesis, the recruitment of neutrophils, and inflammatory pathology; CXCL1 and CXCL3, chemoattractants for neutrophils; interleukin-19 (IL19), which induces the production of IL-6 and TNF 86 ; and CCL20, which is upregulated by TNF 87 . The AT2 cell program included the surfactant proteins, SFTPA1 and SFTPA2; the IL-1 receptor (IL1R1), which may promote antiviral immune responses (below); and, multiple components of MHC-II (e.g., HLA-DPA1, HLA-DPB1), congruent with a role in antigen presentation.
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