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1. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics

Author

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, and Ziegler, Carly G. K.

Published
2021
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3. Human airway mast cells proliferate and acquire distinct inflammation-driven phenotypes during type 2 inflammation

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Koch Institute for Integrative Cancer Research at MIT, Ragon Institute of MGH, MIT and Harvard, Massachusetts Institute of Technology. Computational and Systems Biology Program, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology. Department of Mathematics, Dwyer, Daniel F, Ordovas-Montanes, Jose, Allon, Samuel J, Buchheit, Kathleen M, Vukovic, Marko, Derakhshan, Tahereh, Feng, Chunli, Lai, Juying, Hughes, Travis K, Nyquist, Sarah K, Giannetti, Matthew P, Berger, Bonnie, Bhattacharyya, Neil, Roditi, Rachel E, Katz, Howard R, Nawijn, Martijn C, Berg, Marijn, van den Berge, Maarten, Laidlaw, Tanya M, Shalek, Alex K, Barrett, Nora A, Boyce, Joshua A, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Koch Institute for Integrative Cancer Research at MIT, Ragon Institute of MGH, MIT and Harvard, Massachusetts Institute of Technology. Computational and Systems Biology Program, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology. Department of Mathematics, Dwyer, Daniel F, Ordovas-Montanes, Jose, Allon, Samuel J, Buchheit, Kathleen M, Vukovic, Marko, Derakhshan, Tahereh, Feng, Chunli, Lai, Juying, Hughes, Travis K, Nyquist, Sarah K, Giannetti, Matthew P, Berger, Bonnie, Bhattacharyya, Neil, Roditi, Rachel E, Katz, Howard R, Nawijn, Martijn C, Berg, Marijn, van den Berge, Maarten, Laidlaw, Tanya M, Shalek, Alex K, Barrett, Nora A, and Boyce, Joshua A

Abstract

Mast cells (MCs) play a pathobiologic role in type 2 (T2) allergic inflammatory diseases of the airway, including asthma and chronic rhinosinusitis with nasal polyposis (CRSwNP). Distinct MC subsets infiltrate the airway mucosa in T2 disease, including subepithelial MCs expressing the proteases tryptase and chymase (MCTC) and epithelial MCs expressing tryptase without chymase (MCT). However, mechanisms underlying MC expansion and the transcriptional programs underlying their heterogeneity are poorly understood. Here, we use flow cytometry and single-cell RNA-sequencing (scRNA-seq) to conduct a comprehensive analysis of human MC hyperplasia in CRSwNP, a T2 cytokine-mediated inflammatory disease. We link discrete cell surface phenotypes to the distinct transcriptomes of CRSwNP MCT and MCTC, which represent polarized ends of a transcriptional gradient of nasal polyp MCs. We find a subepithelial population of CD38highCD117high MCs that is markedly expanded during T2 inflammation. These CD38highCD117high MCs exhibit an intermediate phenotype relative to the expanded MCT and MCTC subsets. CD38highCD117high MCs are distinct from circulating MC progenitors and are enriched for proliferation, which is markedly increased in CRSwNP patients with aspirin-exacerbated respiratory disease, a severe disease subset characterized by increased MC burden and elevated MC activation. We observe that MCs expressing a polyp MCT-like effector program are also found within the lung during fibrotic diseases and asthma, and further identify marked differences between MCTC in nasal polyps and skin. These results indicate that MCs display distinct inflammation-associated effector programs and suggest that in situ MC proliferation is a major component of MC hyperplasia in human T2 inflammation.

Published
2022

4. Cyclin D3 drives inertial cell cycling in dark zone germinal center B cells

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Koch Institute for Integrative Cancer Research at MIT, Ragon Institute of MGH, MIT and Harvard, Pae, Juhee, Ersching, Jonatan, Castro, Tiago BR, Schips, Marta, Mesin, Luka, Allon, Samuel J, Ordovas-Montanes, Jose, Mlynarczyk, Coraline, Melnick, Ari, Efeyan, Alejo, Shalek, Alex K, Meyer-Hermann, Michael, Victora, Gabriel D, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Koch Institute for Integrative Cancer Research at MIT, Ragon Institute of MGH, MIT and Harvard, Pae, Juhee, Ersching, Jonatan, Castro, Tiago BR, Schips, Marta, Mesin, Luka, Allon, Samuel J, Ordovas-Montanes, Jose, Mlynarczyk, Coraline, Melnick, Ari, Efeyan, Alejo, Shalek, Alex K, Meyer-Hermann, Michael, and Victora, Gabriel D

Abstract

© 2020 Pae et al. During affinity maturation, germinal center (GC) B cells alternate between proliferation and somatic hypermutation in the dark zone (DZ) and affinity-dependent selection in the light zone (LZ). This anatomical segregation imposes that the vigorous proliferation that allows clonal expansion of positively selected GC B cells takes place ostensibly in the absence of the signals that triggered selection in the LZ, as if by "inertia."We find that such inertial cycles specifically require the cell cycle regulator cyclin D3. Cyclin D3 dose-dependently controls the extent to which B cells proliferate in the DZ and is essential for effective clonal expansion of GC B cells in response to strong T follicular helper (Tfh) cell help. Introduction into the Ccnd3 gene of a Burkitt lymphoma-associated gain-of-function mutation (T283A) leads to larger GCs with increased DZ proliferation and, in older mice, clonal B cell lymphoproliferation, suggesting that the DZ inertial cell cycle program can be coopted by B cells undergoing malignant transformation.

Published
2022

5. Expression of Foxp3 by T follicular helper cells in end-stage germinal centers

Author

Jacobsen, Johanne T., primary, Hu, Wei, additional, R. Castro, Tiago B., additional, Solem, Sigrid, additional, Galante, Alice, additional, Lin, Zeran, additional, Allon, Samuel J., additional, Mesin, Luka, additional, Bilate, Angelina M., additional, Schiepers, Ariën, additional, Shalek, Alex K., additional, Rudensky, Alexander Y., additional, and Victora, Gabriel D., additional

Published
2021
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6. Human airway mast cells proliferate and acquire distinct inflammation-driven phenotypes during type 2 inflammation

Author

Dwyer, Daniel F., primary, Ordovas-Montanes, Jose, additional, Allon, Samuel J., additional, Buchheit, Kathleen M., additional, Vukovic, Marko, additional, Derakhshan, Tahereh, additional, Feng, Chunli, additional, Lai, Juying, additional, Hughes, Travis K., additional, Nyquist, Sarah K., additional, Giannetti, Matthew P., additional, Berger, Bonnie, additional, Bhattacharyya, Neil, additional, Roditi, Rachel E., additional, Katz, Howard R., additional, Nawijn, Martijn C., additional, Berg, Marijn, additional, van den Berge, Maarten, additional, Laidlaw, Tanya M., additional, Shalek, Alex K., additional, Barrett, Nora A., additional, and Boyce, Joshua A., additional

Published
2021
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7. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues

Author

Ziegler, Carly GK, Allon, Samuel J, Nyquist, Sarah K, Mbano, Ian M, Miao, Vincent N, Tzouanas, Constantine N, Cao, Yuming, Yousif, Ashraf S, Bals, Julia, Hauser, Blake M, Feldman, Jared, Muus, Christoph, Wadsworth, Marc H, Kazer, Samuel W, Hughes, Travis K, Doran, Benjamin, Gatter, G James, Vukovic, Marko, Taliaferro, Faith, Mead, Benjamin E, Guo, Zhiru, Wang, Jennifer P, Gras, Delphine, Plaisant, Magali, Ansari, Meshal, Angelidis, Ilias, Adler, Heiko, Sucre, Jennifer MS, Taylor, Chase J, Lin, Brian, Waghray, Avinash, Mitsialis, Vanessa, Dwyer, Daniel F, Buchheit, Kathleen M, Boyce, Joshua A, Barrett, Nora A, Laidlaw, Tanya M, Carroll, Shaina L, Colonna, Lucrezia, Tkachev, Victor, Peterson, Christopher W, Yu, Alison, Zheng, Hengqi Betty, Gideon, Hannah P, Winchell, Caylin G, Lin, Philana Ling, Bingle, Colin D, Snapper, Scott B, Kropski, Jonathan A, Theis, Fabian J, Schiller, Herbert B, Zaragosi, Laure-Emmanuelle, Barbry, Pascal, Leslie, Alasdair, Kiem, Hans-Peter, Flynn, JoAnne L, Fortune, Sarah M, Berger, Bonnie, Finberg, Robert W, Kean, Leslie S, Garber, Manuel, Schmidt, Aaron G, Lingwood, Daniel, Shalek, Alex K, Ordovas-Montanes, Jose, HCA Lung Biological Network. Electronic Address: Lung-Network@Humancellatlas.Org, HCA Lung Biological Network, Yousif, Ashraf S [0000-0001-9215-3853], Hauser, Blake M [0000-0002-0100-1684], Kazer, Samuel W [0000-0002-7380-9594], Sucre, Jennifer MS [0000-0002-6613-1439], Tkachev, Victor [0000-0001-6011-0576], Zheng, Hengqi Betty [0000-0003-0575-6475], Bingle, Colin D [0000-0002-5405-6988], and Apollo - University of Cambridge Repository

Subjects
Adolescent, Pneumonia, Viral, ACE2, non-human primate, HIV Infections, Peptidyl-Dipeptidase A, Cell Line, ISG, Betacoronavirus, Mice, scRNA-seq, Influenza, Human, Animals, Humans, Tuberculosis, human, Child, Lung, Pandemics, mouse, Cells, Cultured, SARS-CoV-2, Serine Endopeptidases, COVID-19, interferon, Mycobacterium tuberculosis, respiratory system, Macaca mulatta, Up-Regulation, Nasal Mucosa, Enterocytes, Alveolar Epithelial Cells, Interferon Type I, Receptors, Virus, Angiotensin-Converting Enzyme 2, Goblet Cells, Single-Cell Analysis, influenza, Coronavirus Infections
Abstract

There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

Published
2020
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8. SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells and is detected in specific cell subsets across tissues

Author

Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Koch Institute for Integrative Cancer Research at MIT, Ziegler, Carly G.K., Allon, Samuel J., Nyquist, Sarah K., Mbano, Ian M., Miao, Vincent N., Tzouanas, Constantine N., Cao, Yuming, Yousif, Ashraf S., Bals, Julia, Hauser, Blake M., Feldman, Jared, Muus, Christoph, Wadsworth, Marc H., Kazer, Samuel W., Hughes, Travis K., Doran, Benjamin, Gatter, G. James, Vukovic, Marko, Taliaferro, Faith, Mead, Benjamin E., Guo, Zhiru, Wang, Jennifer P., Gras, Delphine, Plaisant, Magali, Ansari, Meshal, Angelidis, Ilias, Adler, Heiko, Sucre, Jennifer M.S., Taylor, Chase J., Lin, Brian, Waghray, Avinash, Mitsialis, Vanessa, Dwyer, Daniel F., Buchheit, Kathleen M., Boyce, Joshua A., Barrett, Nora A., Laidlaw, Tanya M., Carroll, Shaina L., Colonna, Lucrezia, Tkachev, Victor, Peterson, Christopher W., Yu, Alison, Zheng, Hengqi Betty, Gideon, Hannah P., Winchell, Caylin G., Lin, Philana Ling, Bingle, Colin D., Snapper, Scott B., Kropski, Jonathan A., Theis, Fabian J., Schiller, Herbert B., Zaragosi, Laure-Emmanuelle, Barbry, Pascal, Leslie, Alasdair, Kiem, Hans-Peter, Flynn, JoAnne L., Fortune, Sarah M., Berger, Bonnie, Finberg, Robert W., Kean, Leslie S., Garber, Manuel, Schmidt, Aaron G., Lingwood, Daniel, Shalek, Alex K., Ordovas-Montanes, Jose, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Koch Institute for Integrative Cancer Research at MIT, Ziegler, Carly G.K., Allon, Samuel J., Nyquist, Sarah K., Mbano, Ian M., Miao, Vincent N., Tzouanas, Constantine N., Cao, Yuming, Yousif, Ashraf S., Bals, Julia, Hauser, Blake M., Feldman, Jared, Muus, Christoph, Wadsworth, Marc H., Kazer, Samuel W., Hughes, Travis K., Doran, Benjamin, Gatter, G. James, Vukovic, Marko, Taliaferro, Faith, Mead, Benjamin E., Guo, Zhiru, Wang, Jennifer P., Gras, Delphine, Plaisant, Magali, Ansari, Meshal, Angelidis, Ilias, Adler, Heiko, Sucre, Jennifer M.S., Taylor, Chase J., Lin, Brian, Waghray, Avinash, Mitsialis, Vanessa, Dwyer, Daniel F., Buchheit, Kathleen M., Boyce, Joshua A., Barrett, Nora A., Laidlaw, Tanya M., Carroll, Shaina L., Colonna, Lucrezia, Tkachev, Victor, Peterson, Christopher W., Yu, Alison, Zheng, Hengqi Betty, Gideon, Hannah P., Winchell, Caylin G., Lin, Philana Ling, Bingle, Colin D., Snapper, Scott B., Kropski, Jonathan A., Theis, Fabian J., Schiller, Herbert B., Zaragosi, Laure-Emmanuelle, Barbry, Pascal, Leslie, Alasdair, Kiem, Hans-Peter, Flynn, JoAnne L., Fortune, Sarah M., Berger, Bonnie, Finberg, Robert W., Kean, Leslie S., Garber, Manuel, Schmidt, Aaron G., Lingwood, Daniel, Shalek, Alex K., and Ordovas-Montanes, Jose

Abstract

There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2) which causes the disease COVID-19. SARSCoV- 2 spike (S)-protein binds ACE2, and in concert with host proteases, principally TMPRSS2, promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues, and the factors that regulate ACE2 expression, remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 amongst tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discover that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells, and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit speciesspecific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

Published
2020

9. Cyclin D3 drives inertial cell cycling in dark zone germinal center B cells

Author

Pae, Juhee, primary, Ersching, Jonatan, additional, Castro, Tiago B.R., additional, Schips, Marta, additional, Mesin, Luka, additional, Allon, Samuel J., additional, Ordovas-Montanes, Jose, additional, Mlynarczyk, Coraline, additional, Melnick, Ari, additional, Efeyan, Alejo, additional, Shalek, Alex K., additional, Meyer-Hermann, Michael, additional, and Victora, Gabriel D., additional

Published
2020
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10. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues

Author

Ziegler, Carly G.K., primary, Allon, Samuel J., additional, Nyquist, Sarah K., additional, Mbano, Ian M., additional, Miao, Vincent N., additional, Tzouanas, Constantine N., additional, Cao, Yuming, additional, Yousif, Ashraf S., additional, Bals, Julia, additional, Hauser, Blake M., additional, Feldman, Jared, additional, Muus, Christoph, additional, Wadsworth, Marc H., additional, Kazer, Samuel W., additional, Hughes, Travis K., additional, Doran, Benjamin, additional, Gatter, G. James, additional, Vukovic, Marko, additional, Taliaferro, Faith, additional, Mead, Benjamin E., additional, Guo, Zhiru, additional, Wang, Jennifer P., additional, Gras, Delphine, additional, Plaisant, Magali, additional, Ansari, Meshal, additional, Angelidis, Ilias, additional, Adler, Heiko, additional, Sucre, Jennifer M.S., additional, Taylor, Chase J., additional, Lin, Brian, additional, Waghray, Avinash, additional, Mitsialis, Vanessa, additional, Dwyer, Daniel F., additional, Buchheit, Kathleen M., additional, Boyce, Joshua A., additional, Barrett, Nora A., additional, Laidlaw, Tanya M., additional, Carroll, Shaina L., additional, Colonna, Lucrezia, additional, Tkachev, Victor, additional, Peterson, Christopher W., additional, Yu, Alison, additional, Zheng, Hengqi Betty, additional, Gideon, Hannah P., additional, Winchell, Caylin G., additional, Lin, Philana Ling, additional, Bingle, Colin D., additional, Snapper, Scott B., additional, Kropski, Jonathan A., additional, Theis, Fabian J., additional, Schiller, Herbert B., additional, Zaragosi, Laure-Emmanuelle, additional, Barbry, Pascal, additional, Leslie, Alasdair, additional, Kiem, Hans-Peter, additional, Flynn, JoAnne L., additional, Fortune, Sarah M., additional, Berger, Bonnie, additional, Finberg, Robert W., additional, Kean, Leslie S., additional, Garber, Manuel, additional, Schmidt, Aaron G., additional, Lingwood, Daniel, additional, Shalek, Alex K., additional, Ordovas-Montanes, Jose, additional, Banovich, Nicholas, additional, Brazma, Alvis, additional, Desai, Tushar, additional, Duong, Thu Elizabeth, additional, Eickelberg, Oliver, additional, Falk, Christine, additional, Farzan, Michael, additional, Glass, Ian, additional, Haniffa, Muzlifah, additional, Horvath, Peter, additional, Hung, Deborah, additional, Kaminski, Naftali, additional, Krasnow, Mark, additional, Kuhnemund, Malte, additional, Lafyatis, Robert, additional, Lee, Haeock, additional, Leroy, Sylvie, additional, Linnarson, Sten, additional, Lundeberg, Joakim, additional, Meyer, Kerstin, additional, Misharin, Alexander, additional, Nawijn, Martijn, additional, Nikolic, Marko Z., additional, Pe’er, Dana, additional, Powell, Joseph, additional, Quake, Stephen, additional, Rajagopal, Jay, additional, Tata, Purushothama Rao, additional, Rawlins, Emma L., additional, Regev, Aviv, additional, Reyfman, Paul A., additional, Rojas, Mauricio, additional, Rosen, Orit, additional, Saeb-Parsy, Kourosh, additional, Samakovlis, Christos, additional, Schiller, Herbert, additional, Schultze, Joachim L., additional, Seibold, Max A., additional, Shepherd, Douglas, additional, Spence, Jason, additional, Spira, Avrum, additional, Sun, Xin, additional, Teichmann, Sarah, additional, Theis, Fabian, additional, Tsankov, Alexander, additional, van den Berge, Maarten, additional, von Papen, Michael, additional, Whitsett, Jeffrey, additional, Xavier, Ramnik, additional, Xu, Yan, additional, and Zhang, Kun, additional

Published
2020
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11. SARS-CoV-2 Receptor ACE2 is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Enriched in Specific Cell Subsets Across Tissues

Author

Ziegler, Carly, primary, Allon, Samuel J., additional, Nyquist, Sarah K., additional, Mbano, Ian, additional, Miao, Vincent N., additional, Cao, Yuming, additional, Yousif, Ashraf S., additional, Bals, Julia, additional, Hauser, Blake M., additional, Feldman, Jared, additional, Muus, Christoph, additional, Wadsworth II, Marc H., additional, Kazer, Samuel, additional, Hughes, Travis K., additional, Doran, Benjamin, additional, Gatter, G. James, additional, Vukovic, Marko, additional, Tzouanas, Constantine N., additional, Taliaferro, Faith, additional, Guo, Zhiru, additional, Wang, Jennifer P., additional, Dwyer, Daniel F., additional, Buchheit, Kathleen M., additional, Boyce, Joshua, additional, Barrett, Nora A., additional, Laidlaw, Tanya M., additional, Carroll, Shaina L., additional, Colonna, Lucrezia, additional, Tkachev, Victor, additional, Yu, Alison, additional, Zheng, Henqi Betty, additional, Gideon, Hannah P., additional, Winchell, Caylin G., additional, Lin, Philana L., additional, Berger, Bonnie, additional, Leslie, Alasdair, additional, Flynn, JoAnne L., additional, Fortune, Sarah M., additional, Finberg, Robert W., additional, Kean, Leslie, additional, Garber, Manuel, additional, Schmidt, Aaron, additional, Lingwood, Daniel, additional, Shalek, Alex K., additional, Ordovas-Montanes, Jose, additional, and Lung Biological Network, HCA, additional

Published
2020
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12. Loss of DNA methyltransferase activity in primed human ES cells triggers increased cell-cell variability and transcriptional repression

Author

Tsankov, Alexander M., primary, Wadsworth, Marc H., additional, Akopian, Veronika, additional, Charlton, Jocelyn, additional, Allon, Samuel J., additional, Arczewska, Aleksandra, additional, Mead, Benjamin E., additional, Drake, Riley S., additional, Smith, Zachary D., additional, Mikkelsen, Tarjei S., additional, Shalek, Alex K., additional, and Meissner, Alexander, additional

Published
2019
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14. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics

Author

Christoph, Muus, Luecken , Malte D., Gökcen, Eraslan, Lisa, Sikkema, Avinash, Waghray, Graham, Heimberg, Yoshihiko, Kobayashi, Eeshit Dhaval Vaishnav, Ayshwarya, Subramanian, Christopher, Smillie, Jagadeesh, Karthik A., Elizabeth Thu Duong, Evgenij, Fiskin, Elena Torlai Triglia, Meshal, Ansari, Peiwen, Cai, Brian, Lin, Justin, Buchanan, Sijia, Chen, Jian, Shu, Haber, Adam L., Hattie, Chung, Montoro, Daniel T., Taylor, Adams, Hananeh, Aliee, Allon, Samuel J., Zaneta, Andrusivova, Ilias, Angelidis, Orr, Ashenberg, Kevin, Bassler, Christophe, Bécavin, Inbal, Benhar, Joseph, Bergenstråhle, Ludvig, Bergenstråhle, Liam, Bolt, Emelie, Braun, Bui, Linh T., Steven, Callori, Mark, Chaffin, Evgeny, Chichelnitskiy, Joshua, Chiou, Conlon, Thomas M., Cuoco, Michael S., Cuomo, Anna S. E., Marie, Deprez, Grant, Duclos, Denise, Fine, Fischer, David S., Shila, Ghazanfar, Astrid, Gillich, Bruno, Giotti, Joshua, Gould, Minzhe, Guo, Gutierrez, Austin J., Habermann, Arun C., Tyler, Harvey, Peng, He, Xiaomeng, Hou, Lijuan, Hu, Yan, Hu, Alok, Jaiswal, Lu, Ji, Peiyong, Jiang, Kapellos, Theodoros S., Kuo, Christin S., Ludvig, Larsson, Leney-Greene, Michael A., Kyungtae, Lim, Monika, Litviňuková, Ludwig, Leif S., Soeren, Lukassen, Wendy, Luo, Henrike, Maatz, Elo, Madissoon, Lira, Mamanova, Kasidet, Manakongtreecheep, Sylvie, Leroy, Mayr, Christoph H., Mbano, Ian M., Mcadams, Alexi M., Nabhan, Ahmad N., Nyquist, Sarah K., Lolita, Penland, Poirion, Olivier B., Sergio, Poli, Cancan, Qi, Rachel, Queen, Daniel, Reichart, Ivan, Rosas, Schupp, Jonas C., Shea, Conor V., Xingyi, Shi, Rahul, Sinha, Sit, Rene V., Kamil, Slowikowski, Michal, Slyper, Smith, Neal P., Alex, Sountoulidis, Maximilian, Strunz, Sullivan, Travis B., Dawei, Sun, Carlos, Talavera-López, Peng, Tan, Jessica, Tantivit, Travaglini, Kyle J., Tucker, Nathan R., Vernon, Katherine A., Wadsworth, Marc H., Julia, Waldman, Xiuting, Wang, Ke, Xu, Wenjun, Yan, William, Zhao, Ziegler, Carly G. K., The NHLBI LungMap Consortium, Zerti, Darin, The Human Cell Atlas Lung Biological Network, and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
0301 basic medicine, Male, Cathepsin L, Respiratory System, Datasets as Topic, Lung/metabolism, Sequence Analysis, RNA/methods, Organ Specificity/genetics, 0302 clinical medicine, 80 and over, Respiratory system, Lung, COVID-19/epidemiology, Aged, 80 and over, Serine Endopeptidases, General Medicine, respiratory system, Middle Aged, Host-Pathogen Interactions/genetics, 3. Good health, Angiotensin-Converting Enzyme 2/genetics, medicine.anatomical_structure, Datasets as Topic/statistics & numerical data, Respiratory System/metabolism, Organ Specificity, Cathepsin L/genetics, 030220 oncology & carcinogenesis, Host-Pathogen Interactions, Tumor necrosis factor alpha, Female, Angiotensin-Converting Enzyme 2, Single-Cell Analysis, RNA/methods, Sequence Analysis, Adult, Alveolar Epithelial Cells/metabolism, Serine Endopeptidases/genetics, Biology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Immune system, Viral entry, Parenchyma, medicine, Humans, Gene Expression Profiling/statistics & numerical data, Aged, Demography, SARS-CoV-2, Sequence Analysis, RNA, Gene Expression Profiling, Single-Cell Analysis/methods, COVID-19, Virus Internalization, Gene expression profiling, 030104 developmental biology, Alveolar Epithelial Cells, Immunology, Tissue tropism, SARS-CoV-2/physiology
Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing 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 type 2 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 interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

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15. Cyclin D3 drives inertial cell cycling in dark zone germinal center B cells

Author

Pae, Juhee, Ersching, Jonatan, Castro, Tiago B.R., Schips, Marta, Mesin, Luka, Allon, Samuel J., Ordovas-Montanes, Jose, Mlynarczyk, Coraline, Melnick, Ari, Efeyan, Alejo, Shalek, Alex K., Meyer-Hermann, Michael, and Victora, Gabriel D.

Abstract

During affinity maturation, germinal center (GC) B cells alternate between proliferation and somatic hypermutation in the dark zone (DZ) and affinity-dependent selection in the light zone (LZ). This anatomical segregation imposes that the vigorous proliferation that allows clonal expansion of positively selected GC B cells takes place ostensibly in the absence of the signals that triggered selection in the LZ, as if by “inertia.” We find that such inertial cycles specifically require the cell cycle regulator cyclin D3. Cyclin D3 dose-dependently controls the extent to which B cells proliferate in the DZ and is essential for effective clonal expansion of GC B cells in response to strong T follicular helper (Tfh) cell help. Introduction into the Ccnd3 gene of a Burkitt lymphoma–associated gain-of-function mutation (T283A) leads to larger GCs with increased DZ proliferation and, in older mice, clonal B cell lymphoproliferation, suggesting that the DZ inertial cell cycle program can be coopted by B cells undergoing malignant transformation.

Published
2021
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