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375 results on '"Geissmann, Frederic"'

1. Plasma membrane abundance dictates phagocytic capacity and functional cross-talk in myeloid cells

Author

Winer, Benjamin Y, Settle, Alexander H, Yakimov, Alexandrina M, Jeronimo, Carlos, Lazarov, Tomi, Tipping, Murray, Saoi, Michelle, Sawh, Anjelique, Sepp, Anna-Liisa L, Galiano, Michael, Perry, Justin SA, Wong, Yung Yu, Geissmann, Frederic, Cross, Justin, Zhou, Ting, Kam, Lance C, Pasolli, H Amalia, Hohl, Tobias, Cyster, Jason G, Weiner, Orion D, and Huse, Morgan

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Cancer, 2.1 Biological and endogenous factors, Animals, Phagocytosis, Cell Membrane, Mice, Mice, Knockout, Myeloid Cells, Mice, Inbred C57BL, Neutrophils, Macrophages, Clinical sciences
Abstract

Professional phagocytes like neutrophils and macrophages tightly control what they consume, how much they consume, and when they move after cargo uptake. We show that plasma membrane abundance is a key arbiter of these cellular behaviors. Neutrophils and macrophages lacking the G protein subunit Gβ4 exhibited profound plasma membrane expansion, accompanied by marked reduction in plasma membrane tension. These biophysical changes promoted the phagocytosis of bacteria, fungus, apoptotic corpses, and cancer cells. We also found that Gβ4-deficient neutrophils are defective in the normal inhibition of migration following cargo uptake. Sphingolipid synthesis played a central role in these phenotypes by driving plasma membrane accumulation in cells lacking Gβ4. In Gβ4 knockout mice, neutrophils not only exhibited enhanced phagocytosis of inhaled fungal conidia in the lung but also increased trafficking of engulfed pathogens to other organs. Together, these results reveal an unexpected, biophysical control mechanism central to myeloid functional decision-making.

Published
2024

4. Diet-regulated production of PDGFcc by macrophages controls energy storage

Author

Cox, Nehemiah, Crozet, Lucile, Holtman, Inge R, Loyher, Pierre-Louis, Lazarov, Tomi, White, Jessica B, Mass, Elvira, Stanley, E Richard, Elemento, Olivier, Glass, Christopher K, and Geissmann, Frederic

Subjects
Genetics, Nutrition, Obesity, Underpinning research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Metabolic and endocrine, Affordable and Clean Energy, Adipocytes, Adipose Tissue, Brown, Animals, Diet, High-Fat, Drosophila Proteins, Drosophila melanogaster, Energy Metabolism, Female, Hemocytes, Liver, Lymphokines, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Platelet-Derived Growth Factor, Receptors, CCR2, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Thermogenesis, Vascular Endothelial Growth Factor A, General Science & Technology
Abstract

The mechanisms by which macrophages regulate energy storage remain poorly understood. We identify in a genetic screen a platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF)-family ortholog, Pvf3, that is produced by macrophages and is required for lipid storage in fat-body cells of Drosophila larvae. Genetic and pharmacological experiments indicate that the mouse Pvf3 ortholog PDGFcc, produced by adipose tissue-resident macrophages, controls lipid storage in adipocytes in a leptin receptor- and C-C chemokine receptor type 2-independent manner. PDGFcc production is regulated by diet and acts in a paracrine manner to control lipid storage in adipose tissues of newborn and adult mice. At the organismal level upon PDGFcc blockade, excess lipids are redirected toward thermogenesis in brown fat. These data identify a macrophage-dependent mechanism, conducive to the design of pharmacological interventions, that controls energy storage in metazoans.

Published
2021

5. Liver-Derived Signals Sequentially Reprogram Myeloid Enhancers to Initiate and Maintain Kupffer Cell Identity

Author

Sakai, Mashito, Troutman, Ty D, Seidman, Jason S, Ouyang, Zhengyu, Spann, Nathanael J, Abe, Yohei, Ego, Kaori M, Bruni, Cassi M, Deng, Zihou, Schlachetzki, Johannes CM, Nott, Alexi, Bennett, Hunter, Chang, Jonathan, Vu, BaoChau T, Pasillas, Martina P, Link, Verena M, Texari, Lorane, Heinz, Sven, Thompson, Bonne M, McDonald, Jeffrey G, Geissmann, Frederic, and Glass, Christopher K

Subjects
Biomedical and Clinical Sciences, Immunology, Genetics, Liver Disease, Stem Cell Research, Human Genome, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Underpinning research, Animals, Cell Differentiation, Cells, Cultured, Cellular Microenvironment, Cellular Reprogramming, Immunoglobulin J Recombination Signal Sequence-Binding Protein, Intracellular Signaling Peptides and Proteins, Kupffer Cells, Liver, Liver X Receptors, Macrophages, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Transgenic, Myeloid Cells, Phenotype, Signal Transduction, Transforming Growth Factor beta
Abstract

Tissue environment plays a powerful role in establishing and maintaining the distinct phenotypes of resident macrophages, but the underlying molecular mechanisms remain poorly understood. Here, we characterized transcriptomic and epigenetic changes in repopulating liver macrophages following acute Kupffer cell depletion as a means to infer signaling pathways and transcription factors that promote Kupffer cell differentiation. We obtained evidence that combinatorial interactions of the Notch ligand DLL4 and transforming growth factor-b (TGF-β) family ligands produced by sinusoidal endothelial cells and endogenous LXR ligands were required for the induction and maintenance of Kupffer cell identity. DLL4 regulation of the Notch transcriptional effector RBPJ activated poised enhancers to rapidly induce LXRα and other Kupffer cell lineage-determining factors. These factors in turn reprogrammed the repopulating liver macrophage enhancer landscape to converge on that of the original resident Kupffer cells. Collectively, these findings provide a framework for understanding how macrophage progenitor cells acquire tissue-specific phenotypes.

Published
2019

6. Clonal Hematopoiesis Is Associated With Long-Term Adverse Outcomes Following Cardiac Surgery.

Author

Ninni, Sandro, Vicario, Rocio, Coisne, Augustin, Woitrain, Eloise, Tazibet, Amine, Stewart, Caitlin M., Diaz Jr, Luis A., White, James Robert, Koussa, Mohammed, Dubrulle, Henri, Juthier, Francis, Jungling, Marie, Vincentelli, André, Edme, Jean-Louis, Nattel, Stanley, de Winther, Menno, Geissmann, Frederic, Dombrowicz, David, Staels, Bart, and Montaigne, David

Published
2024
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9. Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms

Author

Durham, Benjamin H., Lopez Rodrigo, Estibaliz, Picarsic, Jennifer, Abramson, David, Rotemberg, Veronica, De Munck, Steven, Pannecoucke, Erwin, Lu, Sydney X., Pastore, Alessandro, Yoshimi, Akihide, Mandelker, Diana, Ceyhan-Birsoy, Ozge, Ulaner, Gary A., Walsh, Michael, Yabe, Mariko, Petrova-Drus, Kseniya, Arcila, Maria E., Ladanyi, Marc, Solit, David B., Berger, Michael F., Hyman, David M., Lacouture, Mario E., Erickson, Caroline, Saganty, Ruth, Ki, Michelle, Dunkel, Ira J., Santa-María López, Vicente, Mora, Jaume, Haroche, Julien, Emile, Jean-Francois, Decaux, Olivier, Geissmann, Frederic, Savvides, Savvas N., Drilon, Alexander, Diamond, Eli L., and Abdel-Wahab, Omar

Published
2019
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10. Environment Drives Selection and Function of Enhancers Controlling Tissue-Specific Macrophage Identities

Author

Gosselin, David, Link, Verena M, Romanoski, Casey E, Fonseca, Gregory J, Eichenfield, Dawn Z, Spann, Nathanael J, Stender, Joshua D, Chun, Hyun B, Garner, Hannah, Geissmann, Frederic, and Glass, Christopher K

Subjects
Biochemistry and Cell Biology, Genetics, Biological Sciences, Human Genome, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Underpinning research, Aetiology, Inflammatory and immune system, Animals, Enhancer Elements, Genetic, Genetic Variation, Histone Code, Macrophages, Male, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Inbred Strains, Transcription Factors, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Macrophages reside in essentially all tissues of the body and play key roles in innate and adaptive immune responses. Distinct populations of tissue macrophages also acquire context-specific functions that are important for normal tissue homeostasis. To investigate mechanisms responsible for tissue-specific functions, we analyzed the transcriptomes and enhancer landscapes of brain microglia and resident macrophages of the peritoneal cavity. In addition, we exploited natural genetic variation as a genome-wide "mutagenesis" strategy to identify DNA recognition motifs for transcription factors that promote common or subset-specific binding of the macrophage lineage-determining factor PU.1. We find that distinct tissue environments drive divergent programs of gene expression by differentially activating a common enhancer repertoire and by inducing the expression of divergent secondary transcription factors that collaborate with PU.1 to establish tissue-specific enhancers. These findings provide insights into molecular mechanisms by which tissue environment influences macrophage phenotypes that are likely to be broadly applicable to other cell types.

Published
2014

11. Breast Cancer Macrophage Heterogeneity and Self-renewal are Determined by Spatial Localization

Author

Ben-Chetrit, Nir, primary, Niu, Xiang, additional, Sotelo, Jesus, additional, Swett, Ariel D., additional, Rajasekhar, Vinagolu K., additional, Jiao, Maria S., additional, Stewart, Caitlin M., additional, Bhardwaj, Priya, additional, Kottapalli, Sanjay, additional, Ganesan, Saravanan, additional, Loyher, Pierre-Louis, additional, Potenski, Catherine, additional, Hannuna, Assaf, additional, Brown, Kristy A., additional, Iyengar, Neil M., additional, Giri, Dilip D., additional, Lowe, Scott W., additional, Healey, John H., additional, Geissmann, Frederic, additional, Sagi, Irit, additional, Joyce, Johanna A., additional, and Landau, Dan A., additional

Published
2023
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13. Plasma membrane abundance dictates phagocytic capacity and functional crosstalk in myeloid cells

Author

Winer, Benjamin Yana, primary, Settle, Alexander H, additional, Yakimov, Alexandrina M, additional, Jeronimo, Carlos, additional, Lazarovt, Tomi, additional, Tipping, Murray, additional, Saoi, Michelle, additional, Sawh, Anjelique, additional, Sepp, Anna-Liisa L, additional, Galiano, Michael, additional, Perry, Justin Shaun Arnold, additional, Wong, Yung Yu, additional, Geissmann, Frederic, additional, Cross, Justin, additional, Zhou, Ting, additional, Kam, Lance C, additional, Pasoli, Hilda Amalia, additional, Hohl, Tobias, additional, Cyster, Jason G, additional, Weiner, Orion, additional, and Huse, Morgan, additional

Published
2023
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16. Early life high fructose exposure disrupts microglia function and impedes neurodevelopment

Author

Perry, Justin, primary, Wang, Zhaoquan, additional, Lipschutz, Allie, additional, Liu, Zong-Lin, additional, Trzeciak, Alissa, additional, Miranda, Isabella, additional, Martinez de la Torre, Celia, additional, Schild, Tanya, additional, Lazarov, Tomi, additional, Rojas, Waleska Saitz, additional, Saavedra, Pedro, additional, Romero-Pichardo, Jesus, additional, Baako, Ann, additional, Geissmann, Frederic, additional, Faraco, Giuseppe, additional, Gan, Li, additional, Etchegaray, Jon Iker, additional, Lucas, Christopher, additional, Parkhurst, Christopher, additional, Zeng, Melody, additional, and Keshari, Kayvan, additional

Published
2023
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19. Hematopoietic Somatic Mosaicism Is Associated With an Increased Risk of Postoperative Atrial Fibrillation

Author

Ninni, Sandro, primary, Dombrowicz, David, additional, Kuznetsova, Tanya, additional, Vicario, Rocio, additional, Gao, Vance, additional, Molendi-Coste, Olivier, additional, Haas, Joel, additional, Woitrain, Eloise, additional, Coisne, Augustin, additional, Neele, Annette E., additional, Prange, Koen, additional, Willemsen, Lisa, additional, Aghezzaf, Samy, additional, Fragkogianni, Stamatina, additional, Tazibet, Amine, additional, Pineau, Laurent, additional, White, James Robert, additional, Eeckhoute, Jérôme, additional, Koussa, Mohamed, additional, Dubrulle, Henri, additional, Juthier, Francis, additional, Soquet, Jérôme, additional, Vincentelli, André, additional, Edme, Jean-Louis, additional, de Winther, Menno, additional, Geissmann, Frederic, additional, Staels, Bart, additional, and Montaigne, David, additional

Published
2023
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20. Inborn errors of OAS-RNase L in SARS-CoV-2-related multisystem inflammatory syndrome in children

Author

Howard Hughes Medical Institute, Rockefeller University, St. Giles Foundation, National Institutes of Health (US), Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Fundación Mapfre, Cabildo de Tenerife, Fundació La Marató de TV3, Centro de Investigación Biomédica en Red Enfermedades Raras (España), Consejo Superior de Investigaciones Científicas (España), European Commission, Pérez-Tur, Jordi [0000-0002-9111-1712], Lee, Danyel, Le Pen, Jeremie, Yatim, Ahmad, Dong, Beihua, Aquino, Yann, Ogishi, Masato, Pescarmona, Remi, Talouarn, Estelle, Rinchai, Darawan, Zhang, Peng, Perret, Magali, Rice, Charles M., Silverman, Robert H., Zhang, Shen-Ying, Casanova, Jean-Laurent, Liu, Zhiyong, Jordan, Iolanda, Bozdemir, Sefika Elmas, Bayhan, Gulsum Iclal, Beaufils, Camille, Bizien, Lucy, Bisiaux, Aurelie, Lei, Weite, Hasan, Milena, Chen, Jie, Gaughan, Christina, Asthana, Abhishek, Libri, Valentina, Luna, Joseph M., Jaffre, Fabrice, Hoffmann, H-Heinrich, Michailidis, Eleftherios, Moreews, Marion, Seeleuthner, Yoann, Bilguvar, Kaya, Mane, Shrikant, Flores, Carlos, Zhang, Yu, Arias, Andres A., Bailey, Rasheed, Schluter, Agatha, Milisavljevic, Baptiste, Bigio, Benedetta, Le Voyer, Tom, Materna, Marie, Gervais, Adrian, Moncada-Velez, Marcela, Pala, Francesca, Lazarov, Tomi, Levy, Romain, Neehus, Anna-Lena, Rosain, Jeremie, Peel, Jessica, Chan, Yi-Hao, Morin, Marie-Paule, Pino-Ramírez, Rosa María, Belkaya, Serkan, Lorenzo, Lazaro, Anton, Jordi, Delafontaine, Selket, Toubiana, Julie, Bajolle, Fanny, Fumado, Victoria, DeDiego, Marta L., Fidouh, Nadhira, Rozenberg, Flore, Pérez-Tur, Jordi, Chen, Shuibing, Evans, Todd, Geissmann, Frederic, Lebon, Pierre, Weiss, Susan R., Bonnet, Damien, Duval, Xavier, Pan-Hammarström, Qiang, Planas, Anna M., Meyts, Isabelle, Haerynck, Filomeen, Pujol, Aurora, Sancho-Shimizu, Vanessa, Dalgard, Clifford L., Bustamante, Jacinta, Puel, Anne, Boisson-Dupuis, Stéphanie, Boisson, Bertrand, Maniatis, Tom, Zhang, Qian, Bastard, Paul, Notarangelo, Luigi, Beziat, Vivien, Pérez de Diego, Rebeca, Rodriguez-Gallego, Carlos, Su, Helen C., Lifton, Richard P, Jouanguy, Emmanuelle, Cobat, Aurelie, Alsina, Laia, Keles, Sevgi, Haddad, Elie, Abel, Laurent, Belot, Alexandre, Quintana-Murci, Lluis, Howard Hughes Medical Institute, Rockefeller University, St. Giles Foundation, National Institutes of Health (US), Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Fundación Mapfre, Cabildo de Tenerife, Fundació La Marató de TV3, Centro de Investigación Biomédica en Red Enfermedades Raras (España), Consejo Superior de Investigaciones Científicas (España), European Commission, Pérez-Tur, Jordi [0000-0002-9111-1712], Lee, Danyel, Le Pen, Jeremie, Yatim, Ahmad, Dong, Beihua, Aquino, Yann, Ogishi, Masato, Pescarmona, Remi, Talouarn, Estelle, Rinchai, Darawan, Zhang, Peng, Perret, Magali, Rice, Charles M., Silverman, Robert H., Zhang, Shen-Ying, Casanova, Jean-Laurent, Liu, Zhiyong, Jordan, Iolanda, Bozdemir, Sefika Elmas, Bayhan, Gulsum Iclal, Beaufils, Camille, Bizien, Lucy, Bisiaux, Aurelie, Lei, Weite, Hasan, Milena, Chen, Jie, Gaughan, Christina, Asthana, Abhishek, Libri, Valentina, Luna, Joseph M., Jaffre, Fabrice, Hoffmann, H-Heinrich, Michailidis, Eleftherios, Moreews, Marion, Seeleuthner, Yoann, Bilguvar, Kaya, Mane, Shrikant, Flores, Carlos, Zhang, Yu, Arias, Andres A., Bailey, Rasheed, Schluter, Agatha, Milisavljevic, Baptiste, Bigio, Benedetta, Le Voyer, Tom, Materna, Marie, Gervais, Adrian, Moncada-Velez, Marcela, Pala, Francesca, Lazarov, Tomi, Levy, Romain, Neehus, Anna-Lena, Rosain, Jeremie, Peel, Jessica, Chan, Yi-Hao, Morin, Marie-Paule, Pino-Ramírez, Rosa María, Belkaya, Serkan, Lorenzo, Lazaro, Anton, Jordi, Delafontaine, Selket, Toubiana, Julie, Bajolle, Fanny, Fumado, Victoria, DeDiego, Marta L., Fidouh, Nadhira, Rozenberg, Flore, Pérez-Tur, Jordi, Chen, Shuibing, Evans, Todd, Geissmann, Frederic, Lebon, Pierre, Weiss, Susan R., Bonnet, Damien, Duval, Xavier, Pan-Hammarström, Qiang, Planas, Anna M., Meyts, Isabelle, Haerynck, Filomeen, Pujol, Aurora, Sancho-Shimizu, Vanessa, Dalgard, Clifford L., Bustamante, Jacinta, Puel, Anne, Boisson-Dupuis, Stéphanie, Boisson, Bertrand, Maniatis, Tom, Zhang, Qian, Bastard, Paul, Notarangelo, Luigi, Beziat, Vivien, Pérez de Diego, Rebeca, Rodriguez-Gallego, Carlos, Su, Helen C., Lifton, Richard P, Jouanguy, Emmanuelle, Cobat, Aurelie, Alsina, Laia, Keles, Sevgi, Haddad, Elie, Abel, Laurent, Belot, Alexandre, and Quintana-Murci, Lluis

Abstract

Multisystem inflammatory syndrome in children (MIS-C) is a rare and severe condition that follows benign COVID-19. We report autosomal recessive deficiencies of OAS1, OAS2, or RNASEL in five unrelated children with MIS-C. The cytosolic double-stranded RNA (dsRNA)-sensing OAS1 and OAS2 generate 2'-5'-linked oligoadenylates (2-5A) that activate the single-stranded RNA-degrading ribonuclease L (RNase L). Monocytic cell lines and primary myeloid cells with OAS1, OAS2, or RNase L deficiencies produce excessive amounts of inflammatory cytokines upon dsRNA or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) stimulation. Exogenous 2-5A suppresses cytokine production in OAS1-deficient but not RNase L-deficient cells. Cytokine production in RNase L-deficient cells is impaired by MDA5 or RIG-I deficiency and abolished by mitochondrial antiviral-signaling protein (MAVS) deficiency. Recessive OAS-RNase L deficiencies in these patients unleash the production of SARS-CoV-2-triggered, MAVS-mediated inflammatory cytokines by mononuclear phagocytes, thereby underlying MIS-C

Published
2023

21. Specification of tissue-resident macrophages during organogenesis

Author

Mass, Elvira, Ballesteros, Ivan, Farlik, Matthias, Halbritter, Florian, Günther, Patrick, Crozet, Lucile, Jacome-Galarza, Christian E., Händler, Kristian, Klughammer, Johanna, Kobayashi, Yasuhiro, Gomez-Perdiguero, Elisa, Schultze, Joachim L., Beyer, Marc, Bock, Christoph, and Geissmann, Frederic

Published
2016

22. Life-threatening influenza and impaired interferon amplification in human IRF7 deficiency

Author

Ciancanelli, Michael J., Huang, Sarah X. L., Luthra, Priya, Garner, Hannah, Itan, Yuval, Volpi, Stefano, Lafaille, Fabien G., Trouillet, Céline, Schmolke, Mirco, Albrecht, Randy A., Israelsson, Elisabeth, Lim, Hye Kyung, Casadio, Melina, Hermesh, Tamar, Lorenzo, Lazaro, Leung, Lawrence W., Pedergnana, Vincent, Boisson, Bertrand, Okada, Satoshi, Picard, Capucine, Ringuier, Benedicte, Troussier, Françoise, Chaussabel, Damien, Abel, Laurent, Pellier, Isabelle, Notarangelo, Luigi D., García-Sastre, Adolfo, Basler, Christopher F., Geissmann, Frédéric, Zhang, Shen-Ying, Snoeck, Hans-Willem, and Casanova, Jean-Laurent

Published
2015

25. Origin, fate and dynamics of macrophages at central nervous system interfaces

Author

Goldmann, Tobias, Wieghofer, Peter, Jordão, Marta Joana Costa, Prutek, Fabiola, Hagemeyer, Nora, Frenzel, Kathrin, Amann, Lukas, Staszewski, Ori, Kierdorf, Katrin, Krueger, Martin, Locatelli, Giuseppe, Hochgerner, Hannah, Zeiser, Robert, Epelman, Slava, Geissmann, Frederic, Priller, Josef, Rossi, Fabio M V, Bechmann, Ingo, Kerschensteiner, Martin, Linnarsson, Sten, Jung, Steffen, and Prinz, Marco

Published
2016
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27. RA-MAP, molecular immunological landscapes in early rheumatoid arthritis and healthy vaccine recipients

Author

Isaacs, John D., Brockbank, Sarah, Pedersen, Ayako Wakatsuki, Hilkens, Catharien, Anderson, Amy, Stocks, Philip, Lendrem, Dennis, Tarn, Jessica, Smith, Graham R., Allen, Ben, Casement, John, Diboll, Julie, Harry, Rachel, Cooles, Faye A. H., Cope, Andrew P., Simpson, Gemma, Toward, Ruth, Noble, Hayley, Parke, Angela, Wu, Wing, Clarke, Fiona, Scott, David, Scott, Ian C., Galloway, James, Lempp, Heidi, Ibrahim, Fowzia, Schwank, Samana, Molyneux, Gemma, Lazarov, Tomi, Geissmann, Frederic, Goodyear, Carl S., McInnes, Iain B., Donnelly, Iona, Gilmour, Ashley, Virlan, Aysin Tulunay, Porter, Duncan, Ponchel, Frederique, Emery, Paul, El-Jawhari, Jehan, Parmar, Rekha, McDermott, Michael F., Fisher, Benjamin A., Young, Steve P., Jones, Philip, Raza, Karim, Filer, Andrew, Pitzalis, Costantino, Barnes, Michael R., Watson, David S., Henkin, Rafael, Thorborn, Georgina, Fossati-Jimack, Liliane, Kelly, Stephen, Humby, Frances, Bombardieri, Michele, Rana, Sharmila, Jia, Zhilong, Goldmann, Katriona, Lewis, Myles, Ng, Sandra, Barbosa-Silva, Adriano, Tzanis, Evan, Gallagher-Syed, Amaya, John, Christopher R., Ehrenstein, Michael R., Altobelli, Gioia, Martins, Sandra, Nguyen, Dao, Ali, Humayara, Ciurtin, Coziana, Buch, Maya, Symmons, Deborah, Worthington, Jane, Bruce, Ian N., Sergeant, Jamie C., Verstappen, Suzanne M. M., Stirling, Fiona, Hughes-Morley, Adwoa, Tom, Brian, Farewell, Vernon, Zhong, Yujie, Taylor, Peter C., Buckley, Christopher D., Keidel, Sarah, Cuff, Carolyn, Levesque, Marc, Long, Andrew, Liu, Zheng, Lipsky, Samantha, Harvey, Bohdan, Macoritto, Michael, Hong, Feng, Kaymakcalan, Sukru, Tsuji, Wayne, Sabin, Tony, Ward, Neil, Talbot, Susan, Padhji, Desmond, Sleeman, Matthew, Finch, Donna, Herath, Athula, Lindholm, Catharina, Jenkins, Martin, Ho, Meilien, Hollis, Sally, Marshall, Chris, Parker, Gerry, Page, Matt, Edwards, Hannah, Cuza, Alexandru, Gozzard, Neil, Pandis, Ioannis, Rowe, Anthony, Capdevila, Francisco Bonachela, Loza, Matthew J., Curran, Mark, Verbeeck, Denny, Dan Baker, Mela, Christopher M., Vranic, Ivana, Mela, Catherine T., Wright, Stephen, Rowell, Lucy, Vernon, Emma, Joseph, Nina, Payne, Neil, Rao, Ravi, Binks, Michael, Belson, Alexandra, Ludbrook, Valerie, Hicks, Kirsty, Tipney, Hannah, Ellis, Joanne, Hasan, Samiul, Didierlaurent, Arnaud, Burny, Wivine, Haynes, Andrea, Larminie, Chris, Harris, Ray, Dastros-Pitei, Daniela, Carini, Claudio, Kola, Blerina, Jelinsky, Scott, Hodge, Martin, Maciejewski, Mateusz, Ziemek, Daniel, Schulz-Knappe, Peter, Zucht, Hans-Dieter, Budde, Petra, Coles, Mark, Butler, James A., Read, Simon, and Consortium, The RA-MAP

Subjects
Arthritis, Rheumatoid, Proteomics, Statistics and Probability, Vaccines, Humans, Library and Information Sciences, Statistics, Probability and Uncertainty, Monocytes, Autoantibodies, Biological Specimen Banks, Computer Science Applications, Education, Information Systems
Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disorder with poorly defined aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the peripheral blood immune cell landscape of early, drug naive RA, we performed comprehensive clinical and molecular profiling of 267 RA patients and 52 healthy vaccine recipients for up to 18 months to establish a high quality sample biobank including plasma, serum, peripheral blood cells, urine, genomic DNA, RNA from whole blood, lymphocyte and monocyte subsets. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and autoantibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource offering insights into immune-mediated disease pathogenesis, progression and therapeutic response, ultimately contributing to the development and application of targeted therapies for RA.

Published
2022

29. Tissue-resident macrophages originate from yolk-sac-derived erythro-myeloid progenitors

Author

Perdiguero, Elisa Gomez, Klapproth, Kay, Schulz, Christian, Busch, Katrin, Azzoni, Emanuele, Crozet, Lucile, Garner, Hannah, Trouillet, Celine, de Bruijn, Marella F., Geissmann, Frederic, and Rodewald, Hans-Reimer

Subjects
Hematopoietic stem cells -- Physiological aspects -- Genetic aspects -- Research, Macrophages -- Physiological aspects -- Genetic aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Most haematopoietic cells renew from adult haematopoietic stem cells (HSCs) (1-3), however, macrophages in adult tissues can self-maintain independently of HSCs (4-7). Progenitors with macrophage potential in vitro have been described in the yolk sac before emergence of HSCs (8-13), and fetal macrophages (13-15) can develop independently of Myb (4), a transcription factor required for HSC (16), and can persist in adult tissues (4,17,18). Nevertheless, the origin of adult macrophages and the qualitative and quantitative contributions of HSC and putative non-HSC-derived progenitors are still unclear (19). Here we show in mice that the vast majority of adult tissue-resident macrophages in liver (Kupffer cells), brain (microglia), epidermis (Langerhans cells) and lung (alveolar macrophages) originate from a [Tie2.sup.+] (also known as Tek) cellular pathway generating [Csf1r.sup.+] erythro-myeloid progenitors (EMPs) distinct from HSCs. EMPs develop in the yolk sac at embryonic day (E) 8.5, migrate and colonize the nascent fetal liver before E10.5, and give rise to fetal erythrocytes, macrophages, granulocytes and monocytes until at least E16.5. Subsequently, HSC-derived cells replace erythrocytes, granulocytes and monocytes. Kupffer cells, microglia and Langerhans cells are only marginally replaced in one-year-old mice, whereas alveolar macrophages may be progressively replaced in ageing mice. Our fate-mapping experiments identify, in the fetal liver, a sequence of yolk sac EMP-derived and HSC-derived haematopoiesis, and identify yolk sac EMPs as a common origin for tissue macrophages., Csf1r-expressing cells in the mouse embryo give rise to tissue-resident macrophages in adult tissues (4). To identify in the developing embryo the site of origin of Csf1r-expressing cells, we performed [...]

Published
2015

35. TLR3 Deficiency in Patients with Herpes Simplex Encephalitis

Author

Zhang, Shen-Ying, Jouanguy, Emmanuelle, Ugolini, Sophie, Smahi, Asma, Elain, Gaëlle, Romero, Pedro, Segal, David, Sancho-Shimizu, Vanessa, Lorenzo, Lazaro, Puel, Anne, Picard, Capucine, Chapgier, Ariane, Plancoulaine, Sabine, Titeux, Matthias, Cognet, Céline, von Bernuth, Horst, Ku, Cheng-Lung, Casrouge, Armanda, Zhang, Xin-Xin, Barreiro, Luis, Leonard, Joshua, Hamilton, Claire, Lebon, Pierre, Héron, Bénédicte, Vallée, Louis, Quintana-Murci, Lluis, Hovnanian, Alain, Rozenberd, Flore, Vivier, Eric, Geissmann, Frédéric, Tardieu, Marc, Abel, Laurent, and Casanova, Jean-Laurent

Published
2007
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37. Herpes Simplex Virus Encephalitis in Human UNC-93B Deficiency

Author

Casrouge, Armanda, Zhang, Shen-Ying, Eidenschenk, Céline, Jouanguy, Emmanuelle, Puel, Anne, Yang, Kun, Alcais, Alexandre, Picard, Capucine, Mahfoufi, Nora, Nicolas, Nathalie, Lorenzo, Lazaro, Plancoulaine, Sabine, Sénéchal, Brigitte, Geissmann, Frédéric, Tabeta, Koichi, Hoebe, Kasper, Du, Xin, Miller, Richard L., Héron, Bénédicte, Mignot, Cyril, de Villemeur, Thierry Billette, Lebon, Pierre, Dulac, Olivier, Rozenberg, Flore, Beutler, Bruce, Tardieu, Marc, Abel, Laurent, and Casanova, Jean-Laurent

Published
2006
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40. Partial MCM4 deficiency in patients with growth retardation, adrenal insufficiency, and natural killer cell deficiency

Author

Gineau, Laure, Cognet, Celine, Kara, Nihan, Lach, Francis Peter, Dunne, Jean, Veturi, Uma, Picard, Capucine, Trouillet, Celine, Eidenschenk, Celine, Aoufouchi, Said, Alcais, Alexandre, Smith, Owen, Geissmann, Frederic, Feighery, Conleth, Abel, Laurent, Smogorzewska, Agata, Stillman, Bruce, Vivier, Eric, Casanova, Jean-Laurent, and Jouanguy, Emmanuelle

Subjects
Leukocyte disorders -- Risk factors -- Genetic aspects, Gene mutations -- Identification and classification, Growth disorders -- Risk factors -- Genetic aspects, DNA replication -- Research, Adrenal insufficiency -- Risk factors -- Genetic aspects, Health care industry
Abstract

Natural killer (NK) cells are circulating cytotoxic lymphocytes that exert potent and nonredundant antiviral activity and antitumoral activity in the mouse; however, their function in host defense in humans remains unclear. Here, we investigated 6 related patients with autosomal recessive growth retardation, adrenal insufficiency, and a selective NK cell deficiency characterized by a lack of the [CD56.sup.dim] NK subset. Using linkage analysis and fine mapping, we identified the disease-causing gene, MCM4, which encodes a component of the MCM2-7 helicase complex required for DNA replication. A splice-site mutation in the patients produced a frameshift, but the mutation was hypomorphic due to the creation of two new translation initiation methionine codons downstream of the premature termination codon. The patients' fibroblasts exhibited genomic instability, which was rescued by expression of WT MCM4. These data indicate that the patients' growth retardation and adrenal insufficiency likely reflect the ubiquitous but heterogeneous impact of the MCM4 mutation in various tissues. In addition, the specific loss of the NK [CD56.sup.dim] subset in patients was associated with a lower rate of NK [CD56.sup.bright] cell proliferation, and the maturation of NK [CD56.sup.bright] cells toward an NK [CD56.sup.dim] phenotype was tightly dependent on MCM4-dependent cell division. Thus, partial MCM4 deficiency results in a genetic syndrome of growth retardation with adrenal insufficiency and selective NK deficiency., Introduction Natural killer (NK) cells are circulating cytotoxic lymphocytes lacking antigen-specific T cell and B cell receptors (1, 2). They have been shown to exert potent and nonredundant antiviral activity [...]

Published
2012
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45. Expansion of regulatory T cells in patients with Langerhans cell histiocytosis

Author

Senechal, Brigitte, Elain, Gaelle, Jeziorski, Eric, Grondin, Virginie, Patey-Mariaud de Serre, Natacha, Jaubert, Francis, Beldjord, Kheira, Lellouch, Arielle, Glorion, Christophe, Zerah, Michel, Mary, Pierre, Barkaoui, Mohammed, Emile, Jean Francois, Boccon-Gibod, Liliane, Josset, Patrice, Debre, Marianne, Fischer, Alain, Donadieu, Jean, and Geissmann, Frederic

Subjects
T cells -- Research, Langerhans-cell histiocytosis -- Research, Physiology, Pathological -- Observations, Cell proliferation -- Observations
Abstract

ABSTRACT Background Langerhans cell histiocytosis (LCH) is a rare clonal granulomatous disease that affects mainly children. LCH can involve various tissues such as bone, skin, lung, bone marrow, lymph nodes, [...]

Published
2007

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