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Muus, Christoph

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Muus

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Christoph

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Muus, Christoph
Author's Publications: search.filters.isAuthorOfPublication.1ea58936-81fd-4c9d-9c6b-f12962376aab

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    Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics
    (Springer Science and Business Media LLC, 2021-03) Muus, Christoph; Luecken, Malte D.; Eraslan, Gökcen; Sikkema, Lisa; Waghray, Avinash; Heimberg, Graham; Kobayashi, Yoshihiko; Vaishnav, Eeshit Dhaval; Subramanian, Ayshwarya; Smillie, Christopher; Jagadeesh, Karthik A.; Duong, Elizabeth Thu; Fiskin, Evgenij; Torlai Triglia, Elena; Ansari, Meshal; Cai, Peiwen; Lin, Brian; Buchanan, Justin; Chen, Sijia; Shu, Jian; Haber, Adam L.; Chung, Hattie; Montoro, Daniel T.; Adams, Taylor; Aliee, Hananeh; Allon, Samuel J.; Andrusivova, Zaneta; Angelidis, Ilias; Ashenberg, Orr; Bassler, Kevin; Bécavin, Christophe; Benhar, Inbal; Bergenstråhle, Joseph; Bergenstråhle, Ludvig; Bolt, Liam; Braun, Emelie; Bui, Linh T.; Callori, Steven; Chaffin, Mark; Chichelnitskiy, Evgeny; Chiou, Joshua; Conlon, Thomas M.; Cuoco, Michael S.; Cuomo, Anna S. E.; Deprez, Marie; Duclos, Grant; Fine, Denise; Fischer, David S.; Ghazanfar, Shila; Gillich, Astrid; Giotti, Bruno; Gould, Joshua; Guo, Minzhe; Gutierrez, Austin J.; Habermann, Arun C.; Harvey, Tyler; He, Peng; Hou, Xiaomeng; Hu, Lijuan; Hu, Yan; Jaiswal, Alok; Ji, Lu; Jiang, Peiyong; Kapellos, Theodoros S.; Kuo, Christin S.; Larsson, Ludvig; Leney-Greene, Michael A.; Lim, Kyungtae; Litviňuková, Monika; Ludwig, Leif S.; Lukassen, Soeren; Luo, Wendy; Maatz, Henrike; Madissoon, Elo; Mamanova, Lira; Manakongtreecheep, Kasidet; Leroy, Sylvie; Mayr, Christoph H.; Mbano, Ian M.; McAdams, Alexi M.; Nabhan, Ahmad N.; Nyquist, Sarah K.; Penland, Lolita; Poirion, Olivier B.; Poli, Sergio; Qi, CanCan; Queen, Rachel; Reichart, Daniel; Rosas, Ivan; Schupp, Jonas C.; Shea, Conor V.; Shi, Xingyi; Sinha, Rahul; Sit, Rene V.; Slowikowski, Kamil; Slyper, Michal; Smith, Neal P.; Sountoulidis, Alex; Strunz, Maximilian; Sullivan, Travis B.; Sun, Dawei; Talavera-López, Carlos; Tan, Peng; Tantivit, Jessica; Travaglini, Kyle J.; Tucker, Nathan R.; Vernon, Katherine A.; Wadsworth, Marc H.; Waldman, Julia; Wang, Xiuting; Xu, Ke; Yan, Wenjun; Zhao, William; Ziegler, Carly G. K.; Deutsch, Gail H.; Dutra, Jennifer; Gaulton, Kyle J.; Holden-Wiltse, Jeanne; Huyck, Heidie L.; Mariani, Thomas J.; Misra, Ravi S.; Poole, Cory; Preissl, Sebastian; Pryhuber, Gloria S.; Rogers, Lisa; Sun, Xin; Wang, Allen; Whitsett, Jeffrey A.; Xu, Yan; Alladina, Jehan; Banovich, Nicholas E.; Barbry, Pascal; Beane, Jennifer E.; Bhattacharyya, Roby P.; Black, Katharine E.; Brazma, Alvis; Campbell, Joshua D.; Cho, Josalyn L.; Collin, Joseph; Conrad, Christian; de Jong, Kitty; Desai, Tushar; Ding, Diane Z.; Eickelberg, Oliver; Eils, Roland; Ellinor, Patrick T.; Faiz, Alen; Falk, Christine S.; Farzan, Michael; Gellman, Andrew; Getz, Gad; Glass, Ian A.; Greka, Anna; Haniffa, Muzlifah; Hariri, Lida P.; Hennon, Mark W.; Horvath, Peter; Hübner, Norbert; Hung, Deborah T.; Janssen, William J.; Juric, Dejan; Kaminski, Naftali; Koenigshoff, Melanie; Koppelman, Gerard H.; Krasnow, Mark A.; Kropski, Jonathan A.; Kuhnemund, Malte; Lafyatis, Robert; Lako, Majlinda; Lander, Eric S.; Lee, Haeock; Lenburg, Marc E.; Marquette, Charles-Hugo; Metzger, Ross J.; Linnarsson, Sten; Liu, Gang; Lo, Yuk Ming Dennis; Lundeberg, Joakim; Marioni, John C.; Mazzilli, Sarah A.; Medoff, Benjamin D.; Meyer, Kerstin B.; Miao, Zhichao; Misharin, Alexander V.; Nawijn, Martijn C.; Nikolić, Marko Z.; Noseda, Michela; Ordovas-Montanes, Jose; Oudit, Gavin Y.; Pe’er, Dana; Powell, Joseph E.; Quake, Stephen R.; Rajagopal, Jayaraj; Tata, Purushothama Rao; Rawlins, Emma L.; Regev, Aviv; Reid, Mary E.; Reyfman, Paul A.; Rieger-Christ, Kimberly M.; Rojas, Mauricio; Rozenblatt-Rosen, Orit; Saeb-Parsy, Kourosh; Samakovlis, Christos; Sanes, Joshua R.; Schiller, Herbert B.; Schultze, Joachim L.; Schwarz, Roland F.; Segre, Ayellet V.; Seibold, Max A.; Seidman, Christine E.; Seidman, Jon G.; Shalek, Alex K.; Shepherd, Douglas P.; Spence, Jason R.; Spira, Avrum; Sundström, Erik; Teichmann, Sarah A.; Theis, Fabian J.; Tsankov, Alexander M.; Vallier, Ludovic; van den Berge, Maarten; Van Zyl, Tave A.; Villani, Alexandra-Chloé; Weins, Astrid; Xavier, Ramnik J.; Yildirim, Ali Önder; Zaragosi, Laure-Emmanuelle; Zerti, Darin; Zhang, Hongbo; Zhang, Kun; Zhang, Xiaohui
    ACE2 and accessory proteases (TMPRSS2, CTSL) are needed for SARS-CoV-2 cellular entry, and their expression may shed light on viral tropism and impact across the body. We assess the cell type-specific expression of ACE2, TMPRSS2, and CTSL across 107 single-cell RNA-Seq studies from different tissues. ACE2, TMPRSS2, and CTSL are co-expressed in specific subsets of respiratory epithelial cells in the nasal passages, airways, and alveoli, and in cells from other organs associated with COVID-19 transmission or pathology. We performed a meta-analysis of 31 lung scRNA-seq studies with 1,320,896 cells from 377 nasal, airway, and lung parenchyma samples from 228 individuals. This revealed cell type specific associations of age, sex, and smoking with expression levels of ACE2, TMPRSS2, and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar AT2 cells. Expression programs shared by ACE2+TMPRSS2+ cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the IL6, IL1, TNF and complement pathways. Cell type-specific expression patterns may contribute to COVID-19 pathogenesis , and our work highlights putative molecular pathways for therapeutic intervention.
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    Skin-resident innate lymphoid cells converge on a pathogenic effector state
    (Springer Science and Business Media LLC, 2021-02-03) Bielecki, Piotr; Riesenfeld, Samantha J.; Hütter, Jan-Christian; Torlai Triglia, Elena; Kowalczyk, Monika S.; Ricardo-Gonzalez, Roberto R.; Lian, Mi; Amezcua Vesely, Maria C.; Kroehling, Lina; Xu, Hao; Slyper, Michal; Muus, Christoph; Ludwig, Leif S.; Christian, Elena; Tao, Liming; Kedaigle, Amanda J.; Steach, Holly R.; York, Autumn G.; Skadow, Mathias H.; Yaghoubi, Parastou; Dionne, Danielle; Jarret, Abigail; McGee, Heather M.; Porter, Caroline B. M.; Licona-Limón, Paula; Bailis, Will; Jackson, Ruaidhrí; Gagliani, Nicola; Gasteiger, Georg; Locksley, Richard M.; Regev, Aviv; Flavell, Richard A.
    Tissue-resident innate lymphoid cells (ILCs) help sustain barrier function and respond to local signals. ILCs are traditionally divided into subsets (ILC1/ILC2/ILC3) based on transcription factors (TFs) and cytokines1. In the skin, disease-specific production of ILC3-associated cytokines IL-17 and IL-22 in response to IL-23 signaling contributes to dermal inflammation in psoriasis. However, it is not known if this response is initiated by pre-committed ILCs or by cell state transitions. Here, we show that psoriasis induction in mice by IL-23 or imiquimod reconfigures a spectrum of skin ILCs, which converge on a pathogenic ILC3-like state. Tissue-resident ILCs were necessary and sufficient, without circulatory ILCs, to drive pathology. Single-cell RNA-seq profiles of skin ILCs along a time course of psoriatic inflammation formed a dense transcriptional continuum, even at steady state, reflecting fluid ILC states, including a naïve/quiescent-like state and an ILC2 effector state. Upon disease induction, the continuum shifted rapidly to span a mixed, ILC3-like subset, expressing both type 2 and 3 cytokines, which we inferred arose via multiple trajectories. We confirmed the transition potential of quiescent and ILC2 states with in vitro experiments, single-cell ATAC-seq, and in vivo fate mapping. Our results highlight the spectrum and flexibility of skin ILC responses, suggesting that immune activities primed in healthy tissues dynamically adapt to provocations and, left unchecked, drive pathological remodeling.
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    Epigenetic Encoding, Heritability and Plasticity of Glioma Transcriptional Cell States
    (Springer Science and Business Media LLC, 2021-09-30) Chaligne, Ronan; Gaiti, Federico; Silverbush, Dana; Schiffman, Joshua S.; Weisman, Hannah R.; Kluegel, Lloyd; Gritsch, Simon; Deochand, Sunil D.; Gonzalez Castro, L. Nicolas; Richman, Alyssa R.; Klughammer, Johanna; Biancalani, Tommaso; Muus, Christoph; Sheridan, Caroline; Alonso, Alicia; Izzo, Franco; Park, Jane; Rozenblatt-Rosen, Orit; Regev, Aviv; Suvà, Mario L.; Landau, Dan A.
    Single cell RNA-sequencing revealed extensive transcriptional cell state diversity in cancer, often observed independently from genetic heterogeneity, raising the central question of how malignant cell states are encoded epigenetically. To address this, we performed multi-omics single-cell profiling – integrating DNA methylation, transcriptome, and genotyping within the same cells – of diffuse gliomas, tumors governed by defined transcriptional cell state diversity. Direct comparison of the epigenetic profiles of distinct cell states revealed key switches for state transitions recapitulating neurodevelopmental trajectories, and highlighted dysregulated epigenetic mechanisms underlying gliomagenesis. We further developed a quantitative framework to measure cell state heritability and transition dynamics based on high resolution lineage trees directly in human samples. We demonstrated heritability of malignant cell states, with key differences in hierarchal vs. plastic cell state architectures in IDH-mutant glioma vs. IDH-wildtype glioblastoma, respectively. This work provides a novel framework anchoring transcriptional cancer cell states in their epigenetic encoding, inheritance and transition dynamics.