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3. Deciphering the transcriptional network of the dendritic cell lineage

Author

Miller, Jennifer C, Brown, Brian D, Shay, Tal, Gautier, Emmanuel L, Jojic, Vladimir, Cohain, Ariella, Pandey, Gaurav, Leboeuf, Marylene, Elpek, Kutlu G, Helft, Julie, Hashimoto, Daigo, Chow, Andrew, Price, Jeremy, Greter, Melanie, Bogunovic, Milena, Bellemare-Pelletier, Angelique, Frenette, Paul S, Randolph, Gwendalyn J, Turley, Shannon J, and Merad, Miriam

Subjects
Genetics, 1.1 Normal biological development and functioning, Underpinning research, Inflammatory and immune system, Cell Differentiation, Cell Lineage, Dendritic Cells, Gene Expression Profiling, Humans, Transcription, Genetic, Immunological Genome Consortium, Immunology
Abstract

Although much progress has been made in the understanding of the ontogeny and function of dendritic cells (DCs), the transcriptional regulation of the lineage commitment and functional specialization of DCs in vivo remains poorly understood. We made a comprehensive comparative analysis of CD8(+), CD103(+), CD11b(+) and plasmacytoid DC subsets, as well as macrophage DC precursors and common DC precursors, across the entire immune system. Here we characterized candidate transcriptional activators involved in the commitment of myeloid progenitor cells to the DC lineage and predicted regulators of DC functional diversity in tissues. We identified a molecular signature that distinguished tissue DCs from macrophages. We also identified a transcriptional program expressed specifically during the steady-state migration of tissue DCs to the draining lymph nodes that may control tolerance to self tissue antigens.

Published
2012

4. Expansion and Activation of CD103+ Dendritic Cell Progenitors at the Tumor Site Enhances Tumor Responses to Therapeutic PD-L1 and BRAF Inhibition

Author

Salmon, Hélène, Idoyaga, Juliana, Rahman, Adeeb, Leboeuf, Marylène, Remark, Romain, Jordan, Stefan, Casanova-Acebes, Maria, Khudoynazarova, Makhzuna, Agudo, Judith, Tung, Navpreet, Chakarov, Svetoslav, Rivera, Christina, Hogstad, Brandon, Bosenberg, Marcus, Hashimoto, Daigo, Gnjatic, Sacha, Bhardwaj, Nina, Palucka, Anna Karolina, Brown, Brian D., Brody, Joshua, Ginhoux, Florent, and Merad, Miriam

Published
2016
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5. Supplemental Figure S3 from Requirement for Innate Immunity and CD90+ NK1.1− Lymphocytes to Treat Established Melanoma with Chemo-Immunotherapy

Author

Moskalenko, Marina, primary, Pan, Michael, primary, Fu, Yichun, primary, de Moll, Ellen H., primary, Hashimoto, Daigo, primary, Mortha, Arthur, primary, Leboeuf, Marylene, primary, Jayaraman, Padmini, primary, Bernardo, Sebastian, primary, Sikora, Andrew G., primary, Wolchok, Jedd, primary, Bhardwaj, Nina, primary, Merad, Miriam, primary, and Saenger, Yvonne, primary

Published
2023
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6. Supplemental Methods from Requirement for Innate Immunity and CD90+ NK1.1− Lymphocytes to Treat Established Melanoma with Chemo-Immunotherapy

Author

Moskalenko, Marina, primary, Pan, Michael, primary, Fu, Yichun, primary, de Moll, Ellen H., primary, Hashimoto, Daigo, primary, Mortha, Arthur, primary, Leboeuf, Marylene, primary, Jayaraman, Padmini, primary, Bernardo, Sebastian, primary, Sikora, Andrew G., primary, Wolchok, Jedd, primary, Bhardwaj, Nina, primary, Merad, Miriam, primary, and Saenger, Yvonne, primary

Published
2023
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7. Supplemental Figure Legends from Requirement for Innate Immunity and CD90+ NK1.1− Lymphocytes to Treat Established Melanoma with Chemo-Immunotherapy

Author

Moskalenko, Marina, primary, Pan, Michael, primary, Fu, Yichun, primary, de Moll, Ellen H., primary, Hashimoto, Daigo, primary, Mortha, Arthur, primary, Leboeuf, Marylene, primary, Jayaraman, Padmini, primary, Bernardo, Sebastian, primary, Sikora, Andrew G., primary, Wolchok, Jedd, primary, Bhardwaj, Nina, primary, Merad, Miriam, primary, and Saenger, Yvonne, primary

Published
2023
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8. Data from Requirement for Innate Immunity and CD90+ NK1.1− Lymphocytes to Treat Established Melanoma with Chemo-Immunotherapy

Author

Moskalenko, Marina, primary, Pan, Michael, primary, Fu, Yichun, primary, de Moll, Ellen H., primary, Hashimoto, Daigo, primary, Mortha, Arthur, primary, Leboeuf, Marylene, primary, Jayaraman, Padmini, primary, Bernardo, Sebastian, primary, Sikora, Andrew G., primary, Wolchok, Jedd, primary, Bhardwaj, Nina, primary, Merad, Miriam, primary, and Saenger, Yvonne, primary

Published
2023
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10. Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress

Author

Hodes, Georgia E., Pfau, Madeline L., Leboeuf, Marylene, Golden, Sam A., Christoffel, Daniel J., Bregman, Dana, Rebusi, Nicole, Heshmati, Mitra, Aleyasin, Hossein, Warren, Brandon L., Lebonté, Benoit, Horn, Sarah, Lapidus, Kyle A., Stelzhammer, Viktoria, Wong, Erik H. F., Bahn, Sabine, Krishnan, Vaishnav, Bolaños-Guzman, Carlos A., Murrough, James W., Merad, Miriam, and Russo, Scott J.

Published
2014

12. Tissue-Resident Macrophages Self-Maintain Locally throughout Adult Life with Minimal Contribution from Circulating Monocytes

Author

Hashimoto, Daigo, Chow, Andrew, Noizat, Clara, Teo, Pearline, Beasley, Mary Beth, Leboeuf, Marylene, Becker, Christian D., See, Peter, Price, Jeremy, Lucas, Daniel, Greter, Melanie, Mortha, Arthur, Boyer, Scott W., Forsberg, E. Camilla, Tanaka, Masato, van Rooijen, Nico, García-Sastre, Adolfo, Stanley, E. Richard, Ginhoux, Florent, Frenette, Paul S., and Merad, Miriam

Published
2013
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15. GM-CSF Controls Nonlymphoid Tissue Dendritic Cell Homeostasis but Is Dispensable for the Differentiation of Inflammatory Dendritic Cells

Author

Greter, Melanie, Helft, Julie, Chow, Andrew, Hashimoto, Daigo, Mortha, Arthur, Agudo-Cantero, Judith, Bogunovic, Milena, Gautier, Emmanuel L., Miller, Jennifer, Leboeuf, Marylene, Lu, Geming, Aloman, Costica, Brown, Brian D., Pollard, Jeffrey W., Xiong, Huabao, Randolph, Gwendalyn J., Chipuk, Jerry E., Frenette, Paul S., and Merad, Miriam

Published
2012
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17. Origin of the Lamina Propria Dendritic Cell Network

Author

Bogunovic, Milena, Ginhoux, Florent, Helft, Julie, Shang, Limin, Hashimoto, Daigo, Greter, Melanie, Liu, Kang, Jakubzick, Claudia, Ingersoll, Molly A., Leboeuf, Marylene, Stanley, E. Richard, Nussenzweig, Michel, Lira, Sergio A., Randolph, Gwendalyn J., and Merad, Miriam

Published
2009
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18. CD169+ macrophages provide a niche promoting erythropoiesis under homeostasis and stress

Author

Chow, Andrew, Huggins, Matthew, Ahmed, Jalal, Hashimoto, Daigo, Lucas, Daniel, Kunisaki, Yuya, Pinho, Sandra, Leboeuf, Marylene, Noizat, Clara, van Rooijen, Nico, Tanaka, Masato, Zhao, Zhizhuang Joe, Bergman, Aviv, Merad, Miriam, and Frenette, Paul S.

Subjects
Physiological aspects, Analysis, Research, Macrophages -- Physiological aspects -- Analysis -- Research, Erythropoiesis -- Physiological aspects -- Analysis -- Research
Abstract

Humans produce millions of erythrocytes each minute, and careful coordination of their production and clearance is crucial to maintain erythropoietic homeostasis. This homeostasis can be challenged by a variety of [...], A role for macrophages in erythropoiesis was suggested several decades ago when erythroblastic islands in the bone marrow, composed of a central macrophage surrounded by developing erythroblasts, were described. However, the in vivo role of macrophages in erythropoiesis under homeostatic conditions or in disease remains unclear. We found that specific depletion of [CD169.sup.+] macrophages markedly reduced the number of erythroblasts in the bone marrow but did not result in overt anemia under homeostatic conditions, probably because of concomitant alterations in red blood cell clearance. However, [CD169.sup.+] macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation. Furthermore, macrophage depletion normalized the erythroid compartment in a [JAK2.sup.V617F]-driven mouse model of polycythemia vera, suggesting that erythropoiesis in polycythemia vera remains under the control of macrophages in the bone marrow and splenic microenvironments. These results indicate that [CD169.sup.+] macrophages promote late erythroid maturation and that modulation of the macrophage compartment may be a new strategy to treat erythropoietic disorders.

Published
2013
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19. Cross-presenting [CD103.sup.+] dendritic cells are protected from influenza virus infection

Author

Helft, Julie, Manicassamy, Balaji, Guermonprez, Pierre, Hashimoto, Daigo, Silvin, Aymeric, Agudo, Judith, Brown, Brian D., Schmolke, Mirco, Miller, Jennifer C., Leboeuf, Marylene, Murphy, Kenneth M., Garcia-Sastre, Adolfo, and Merad, Miriam

Subjects
Prevention, Genetic aspects, Research, Risk factors, CD8 lymphocytes -- Genetic aspects, Influenza -- Risk factors -- Prevention -- Genetic aspects, Dendritic cells -- Genetic aspects, Gene expression -- Research
Abstract

Introduction The identification of the mechanisms that control the initiation of anti-influenza virus [CD8.sup.+] T cell responses that clear viral infections requires knowledge of the identity of the APCs and [...], [CD8.sup.+] cytotoxic T cells are critical for viral clearance from the lungs upon influenza virus infection. The contribution of antigen cross-presentation by DCs to the induction of antiviral cytotoxic T cells remains controversial. Here, we used a recombinant influenza virus expressing a nonstructural 1-GFP (NS1-GFP) reporter gene to visualize the route of antigen presentation by lung DCs upon viral infection in mice. We found that lung [CD103.sup.+] DCs were the only subset of cells that carried intact GFP protein to the draining LNs. Strikingly, lung migratory [CD103.sup.+] DCs were not productively infected by influenza virus and thus were able to induce virus-specific [CD8.sup.+] T cells through the cross-presentation of antigens from virally infected cells. We also observed that [CD103.sup.+] DC resistance to infection correlates with an increased antiviral state in these cells that is dependent on the expression of type I IFN receptor. These results show that efficient cross-priming by migratory lung DCs is coupled to the acquisition of an anti-viral status, which is dependent on the type I IFN signaling pathway.

Published
2012
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20. Stable Isotope Tracing In Vivo Reveals A Metabolic Bridge Linking The Microbiota To Host Histone Acetylation

Author

Lund, Peder J, primary, Gates, Leah A, additional, Leboeuf, Marylene, additional, Smith, Sarah A, additional, Chau, Lillian, additional, Friedman, Elliot S, additional, Lopes, Mariana, additional, Saiman, Yedidya, additional, Kim, Min Soo, additional, Petucci, Christopher, additional, Allis, C. David, additional, Wu, Gary D, additional, and Garcia, Benjamin A, additional

Published
2021
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21. ImmGen at 15

Author

Aguilar, Stephanie Vargas, Aguilar, Oscar, Allan, Rhys, Amir, El Ad David, Angeli, Veronique, Artyomov, Maxim, Asinovski, Natasha, Astarita, Jilian, Austen, K. Frank, Bajpai, Geetika, Barrett, Nora, Baysoy, Alev, Benoist, Christophe, Bellemare-Pelletier, Angelique, Berg, Brad, Best, Adam, Bezman, Natalie, Blair, David, Blander, Julie, Bogunovic, Milena, Brennan, Patrick, Brenner, Michael, Brown, Brian, Buechler, Matthew, Buenrostro, Jason, Casanova, Maria Acebes, Choi, Kyunghee, Chow, Andrew, Chudnovskiy, Aleksey, Cipoletta, Daniela, Cohen, Nadia, Collins, James, Colonna, Marco, Cook, Alison, Costello, James, Cremasco, Viviana, Crowl, Ty, Crozat, Karine, Cruse, Richard, D’angelo, June, Dalod, Marc, Davis, Scott, Demiralp, Cagatay, Deng, Tianda, Desai, Jigar, Desland, Fiona, Dhainaut, Maxime, Ding, Jiarui, Doedens, Andrew, Dominguez, Claudia, Doran, Graeme, Dress, Regine, Dustin, Michael, Dwyer, Daniel, Dzhagalov, Ivan, Elpek, Kutlu, Ergun, Ayla, Ericson, Jeff, Esomonu, Eunice, Fairfax, Keke, Fletcher, Anne, Frascoli, Michela, Fuchs, Anja, Gainullina, Anastasiia, Gal-Oz, Shani, Gallagher, Michael, Gautier, Emmanuel, Gazit, Roi, Gibbings, Sophie, Giraud, Matthieu, Ginhoux, Florent, Goldrath, Ananda, Gotthardt, Dagmar, Gray, Daniel, Greter, Melanie, Grieshaber-Bouyer, Ricardo, Guilliams, Martin, Haidermota, Sara, Hardy, Randy, Hashimoto, Daigo, Helft, Julie, Hendricks, Deborah, Heng, Tracy, Hill, Jonathan, Hyatt, Gordon, Idoyaga, Juliana, Jakubzick, Claudia, Jarjoura, Jessica, Jepson, Daniel, Jia, Baosen, Jianu, Radu, Johanson, Tim, Jordan, Stefan, Jojic, Vladimir, Kamimura, Yosuke, Kana, Veronica, Kang, Joonsoo, Kapoor, Varun, Kenigsberg, Ephriam, Kent, Andrew, Kim, Charles, Kim, Edy, Kim, Francis, Kim, Joel, Kim, Kiwook, Kiner, Evgeny, Knell, Jamie, Koller, Daphne, Kozinn, Larry, Krchma, Karen, Kreslavsky, Taras, Kronenberg, Mitchell, Kwan, Wing-Hong, Laidlaw, David, Lam, Viola, Lanier, Lewis, Laplace, Catherine, Lareau, Caleb, Lavin, Yonit, Lavine, Kory, Leader, Andrew, Leboeuf, Marylene, Lee, Jacob, Lee, Jisu, Li, Bo, Li, Hu, Li, Yuesheng, Lionakis, Michail, Luche, Herve, Lynch, Lydia, Magen, Assaf, Maier, Barbara, Malhotra, Deepali, Malhotra, Nidhi, Malissen, Marie, Maslova, Alexandra, Mathis, Diane, Mcfarland, Adelle, Merad, Miriam, Meunier, Etienne, Miller, Jennifer, Milner, Justin, Mingueneau, Michael, Min-Oo, Gundula, Monach, Paul, Moodley, Devapregasan, Mortha, Arthur, Morvan, Maelig, Mostafavi, Sara, Muller, Soren, Muus, Christoph, Nabekura, Tsukasa, Rao, Tata Nageswara, Narang, Vipin, Narayan, Kavitha, Ner-Gaon, Hadas, Nguyen, Quyhn, Nigrovic, Peter, Novakovsky, German, Nutt, Stephan, Omilusik, Kayla, Ortiz-Lopez, Adriana, Paidassi, Helena, Paik, Henry, Painter, Michio, Paynich, Mallory, Peng, Vincent, Potempa, Marc, Pradhan, Rachana, Price, Jeremy, Qi, Yilin, Qi, Yiqing, Quon, Sara, Ramirez, Ricardo, Ramanan, Deepshika, Randolph, Gwendalyn, Regev, Aviv, Rhoads, Andrew, Robinette, Michelle, Rose, Samuel, Rossi, Derrick, Rothamel, Katie, Sachidanandam, Ravi, Sathe, Priyanka, Scott, Charlotte, Seddu, Kumba, See, Peter, Sergushichev, Alexey, Shaw, Laura, Shay, Tal, Shemesh, Avishai, Shinton, Susan, Shyer, Justin, Sieweke, Michael, Smillie, Chris, Spel, Lotte, Spidale, Nick, Stifano, Giuseppina, Subramanian, Ayshwarya, Sun, Joseph, Sylvia, Katelyn, Tellier, Julie, This, Sébastien, Tomasello, Elena, Todorov, Helena, Turley, Shannon, Vijaykumar, Brinda, Wagers, Amy, Wakamatsu, Ei, Wang, Chendi, Wang, Peter, Wroblewska, Aleksandra, Wu, Jun, Yang, Edward, Yang, Liang, Yim, Aldrin, Yng, Lim Sheau, Yoshida, Hideyuki, Yu, Bingfei, Zhou, Yan, Zhu, Yanan, Ziemkiewicz, Caroline, Microenvironment, Cell Differentiation, Immunology and Cancer (MICMAC), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), The Walter and Eliza Hall Institute of Medical Research (WEHI), Icahn School of Medicine at Mount Sinai [New York] (MSSM), National University of Singapore (NUS), Washington University School of Medicine in St. Louis, Washington University in Saint Louis (WUSTL), Harvard Medical School [Boston] (HMS), Genentech, Inc. [San Francisco], Brigham & Women’s Hospital [Boston] (BWH), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Brown University, Lymphocytes B effecteurs et à mémoire – Effector and memory B cells, Centre International de Recherche en Infectiologie - UMR (CIRI), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Technische Universität Dresden = Dresden University of Technology (TU Dresden), Crozat, Karine, and Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL)

Subjects
0301 basic medicine, Regulation of gene expression, [SDV.IMM] Life Sciences [q-bio]/Immunology, Test data generation, Computer science, [SDV]Life Sciences [q-bio], Immunology, Gene regulatory network, Genomics, Genome project, Data science, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, microRNA, Immunology and Allergy, DECIPHER, [SDV.IMM]Life Sciences [q-bio]/Immunology, Scientific publishing, ComputingMilieux_MISCELLANEOUS, 030215 immunology
Abstract

International audience; 700 comment | SERIES ImmGen at 15 Nature Immunology's 20 th anniversary is a good opportunity to reminisce about the ImmGen collective endeavor-its goals, successes and horror stories-and the group's exploration of various modes of scientific publishing. The Immunological Genome Project T he Immunological Genome Project (ImmGen) is a collaborative group of immunology and computational biology laboratories that perform a thorough dissection of gene expression and its regulation in the immune system of the mouse. This activity first centered on mRNA expression and then expanded to microRNA (miRNA), chromatin structure, nuclear organization and protein-RNA relationships. Shared protocols, data generation and QC pipelines have yielded data that can be directly compared from >250 stem, lymphoid and myeloid cell types, at baseline or under challenge. The group develops and applies computational tools to decipher regulatory connections and transcriptional control. From its inception, data generated by ImmGen were meant to be a public resource, and they can be accessed through dedicated web and smartphone platforms that use interactive graphic displays that make the results intuitive to users.

Published
2020
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26. P165 INFLUENCE OF THE GUT MICROBIOTA ON COLONIC HISTONE MODIFICATIONS THROUGH BUTYRATE METABOLISM UNDER HEALTHY AND INFLAMMATORY CONDITIONS

Author

Lund, Peder, primary, Smith, Sarah, additional, Simithy, Johayra, additional, Chau, Lillian, additional, Friedman, Elliot, additional, Saiman, Yedidya, additional, Gates, Leah, additional, Leboeuf, Marylene, additional, Trefely, Sophie, additional, Lopes, Mariana, additional, Yuan, Zuo-Fei, additional, Janssen, Kevin, additional, Kim, Min-Soo, additional, Petucci, Christopher, additional, Snyder, Nathaniel, additional, Bewtra, Meena, additional, Allis, C. David, additional, Wu, Gary, additional, and Garcia, Benjamin, additional

Published
2020
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27. The cell cycle inhibitor Cdkn1a regulates Langerhans cell radiation resistance and promotes T regulatory cell generation upon exposure to ionizing irradiation

Author

Price, Jeremy G., Idoyaga, Juliana, Salmon, Hélène, Hogstad, Brandon, Bigarella, Carolina L., Ghaffari, Saghi, Leboeuf, Marylene, and Merad, Miriam

Subjects
Cyclin-Dependent Kinase Inhibitor p21, integumentary system, Langerhans Cells, Radiation, Ionizing, Animals, hemic and immune systems, chemical and pharmacologic phenomena, T-Lymphocytes, Regulatory, Article
Abstract

Treatment with ionizing irradiation (IR) may lead to accumulation of tumor-infiltrating T regulatory (Treg) cells and subsequent tumor resistance to radiotherapy. Here we focused on the contribution of the epidermal mononuclear phagocytes, Langerhans cells (LCs), to this phenomenon because of their ability to resist depletion by high-dose IR. We found that LCs resisted apoptosis and rapidly repaired DNA damage post-IR. Particularly, we found that CDKN1A (cyclin-dependent kinase inhibitor 1A, also known as p21) was overexpressed in LCs, and that Cdkn1a−/− LCs underwent apoptosis and accumulated DNA damage following IR treatment. Wild-type, but not Cdkn1a−/−, LCs up-regulated major histocompatibility complex class II molecules, migrated to the draining lymph nodes and increased Treg cell numbers upon exposure to IR. These findings suggest a means for manipulating LC IR-resistance to increase cutaneous tumor response to radiotherapy.

Published
2015

30. Epigenetic modulation of inflammation and synaptic plasticity promotes resilience against stress in mice

Author

Wang, Jun, Hodes, Georgia E., Zhang, Hongxing, Zhang, Song, Zhao, Wei, Golden, Sam A., Bi, Weina, Menard, Caroline, Kana, Veronika, Leboeuf, Marylene, Xie, Marc, Bregman, Dana, Pfau, Madeline L., Flanigan, Meghan E., Estebam-Fernández, Adelaida, Yemul, Shrishailam, Sharma, Ali, Ho, Lap, Dixon, Richard A., Merad, Miriam, Han, Ming-Hu, Russo, Scott J., Pasinetti, Giulio M., Wang, Jun, Hodes, Georgia E., Zhang, Hongxing, Zhang, Song, Zhao, Wei, Golden, Sam A., Bi, Weina, Menard, Caroline, Kana, Veronika, Leboeuf, Marylene, Xie, Marc, Bregman, Dana, Pfau, Madeline L., Flanigan, Meghan E., Estebam-Fernández, Adelaida, Yemul, Shrishailam, Sharma, Ali, Ho, Lap, Dixon, Richard A., Merad, Miriam, Han, Ming-Hu, Russo, Scott J., and Pasinetti, Giulio M.

Abstract

Major depressive disorder is associated with abnormalities in the brain and the immune system. Chronic stress in animals showed that epigenetic and inflammatory mechanisms play important roles in mediating resilience and susceptibility to depression. Here, through a highthroughput screening, we identify two phytochemicals, dihydrocaffeic acid (DHCA) and malvidin-3′-O-glucoside (Mal-gluc) that are effective in promoting resilience against stress by modulating brain synaptic plasticity and peripheral inflammation. DHCA/Mal-gluc also significantly reduces depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of hematopoietic progenitor cells from stresssusceptible mice. DHCA reduces pro-inflammatory interleukin 6 (IL-6) generations by inhibiting DNA methylation at the CpG-rich IL-6 sequences introns 1 and 3, while Mal-gluc modulates synaptic plasticity by increasing histone acetylation of the regulatory sequences of the Rac1 gene. Peripheral inflammation and synaptic maladaptation are in line with newly hypothesized clinical intervention targets for depression that are not addressed by currently available antidepressants.

Published
2018
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31. CD169+ macrophages provide a niche promoting erythropoiesis under homeostasis, myeloablation and in JAK2V617F-induced polycythemia vera

Author

Chow, Andrew, Huggins, Matthew, Ahmed, Jalal, Hashimoto, Daigo, Lucas, Daniel, Kunisaki, Yuya, Pinho, Sandra, Leboeuf, Marylene, Noizat, Clara, van Rooijen, Nico, Tanaka, Masato, Zhao, Zhizhuang Joe, Bergman, Aviv, Merad, Miriam, and Frenette, Paul S.

Subjects
hemic and lymphatic diseases, Article
Abstract

The role of macrophages in erythropoiesis was suggested several decades ago with the description of “erythroblastic islands” in the bone marrow (BM) composed of a central macrophage surrounded by developing erythroblasts. However, the in vivo role of macrophages in erythropoiesis under homeostasis or disease remains unclear. Specific depletion of CD169+ macrophages markedly reduced erythroblasts in the BM but did not result in overt anemia under homeostasis likely due to concomitant alterations in RBC clearance. However, CD169+ macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation. Furthermore, macrophage depletion normalized the erythroid compartment in a JAK2V617F-driven murine model of polycythemia vera (PV), suggesting that erythropoiesis in PV, unexpectedly, remains under the control of macrophages in the BM and splenic microenvironments. These data indicate that CD169+ macrophages promote late erythroid maturation and that modulation of the macrophage compartment represents a novel strategy to treat erythropoietic disorders.

Published
2013

32. Deciphering the transcriptional network of the DC lineage

Author

Miller, Jennifer C, Brown, Brian D., Shay, Tal, Gautier, Emmanuel L, Jojic, Vladimir, Cohain, Ariella, Pandey, Gaurav, Leboeuf, Marylene, Elpek, Kutlu G, Helft, Julie, Hashimoto, Daigo, Chow, Andrew, Price, Jeremy, Greter, Melanie, Bogunovic, Milena, Bellemare-Pelletier, Angelique, Frenette, Paul S., Randolph, Gwendalyn J., Turley, Shannon J., and Merad, Miriam

Subjects
Article
Abstract

Although, much progress has been made in our understanding of DC ontogeny and function, the transcriptional regulation of DC lineage commitment and functional specialization in vivo is poorly understood. We performed a comprehensive comparative analysis of CD8+, CD103+, CD11b+, and plasmacytoid DC subsets and the recently identified Macrophage DC precursors and Common DC precursors across the entire immune system. Here we characterize candidate transcriptional activators involved in myeloid progenitor commitment to the DC lineage and predicted regulators of DC functional diversity in tissues. We identify a molecular signature that distinguishes tissue DC from macrophages. We also identify a transcriptional program expressed specifically during steady-state tissue DC migration to the draining lymph nodes that may control tolerance to self-tissue antigens.

Published
2012

33. Epigenetic modulation of inflammation and synaptic plasticity promotes resilience against stress in mice

Author

Wang, Jun, primary, Hodes, Georgia E., additional, Zhang, Hongxing, additional, Zhang, Song, additional, Zhao, Wei, additional, Golden, Sam A., additional, Bi, Weina, additional, Menard, Caroline, additional, Kana, Veronika, additional, Leboeuf, Marylene, additional, Xie, Marc, additional, Bregman, Dana, additional, Pfau, Madeline L., additional, Flanigan, Meghan E., additional, Esteban-Fernández, Adelaida, additional, Yemul, Shrishailam, additional, Sharma, Ali, additional, Ho, Lap, additional, Dixon, Richard, additional, Merad, Miriam, additional, Han, Ming-Hu, additional, Russo, Scott J., additional, and Pasinetti, Giulio M., additional

Published
2018
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34. RAF/MEK/extracellular signal–related kinase pathway suppresses dendritic cell migration and traps dendritic cells in Langerhans cell histiocytosis lesions

Author

Hogstad, Brandon, primary, Berres, Marie-Luise, additional, Chakraborty, Rikhia, additional, Tang, Jun, additional, Bigenwald, Camille, additional, Serasinghe, Madhavika, additional, Lim, Karen Phaik Har, additional, Lin, Howard, additional, Man, Tsz-Kwong, additional, Remark, Romain, additional, Baxter, Samantha, additional, Kana, Veronika, additional, Jordan, Stefan, additional, Karoulia, Zoi, additional, Kwan, Wing-hong, additional, Leboeuf, Marylene, additional, Brandt, Elisa, additional, Salmon, Helene, additional, McClain, Kenneth, additional, Poulikakos, Poulikos, additional, Chipuk, Jerry, additional, Mulder, Willem J.M., additional, Allen, Carl E., additional, and Merad, Miriam, additional

Published
2017
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35. Computed tomography of the chest with model-based iterative reconstruction using a radiation exposure similar to chest X-ray examination: preliminary observations

Author

Neroladaki, Angeliki, Botsikas, Diomidis, Boudabbous, Sana, Becker, Christoph, Montet, Xavier Cédric Rodolphe, Leboeuf, Marylene, Becker, Christian D, See, Peter, Price, Jeremy, Lucas, Daniel, Greter, Melanie, Mortha, Arthur, Boyer, Scott W, Forsberg, E Camilla, Tanaka, Masato, van Rooijen, Nico, García-Sastre, Adolfo, Stanley, E Richard, Ginhoux, Florent, Frenette, Paul S, and Merad, Miriam

Subjects
Adult, Male, Quality Control, medicine.medical_specialty, Lung Neoplasms, Image quality, Image Processing, Computer-Assisted/methods, Radiography, Iterative reconstruction, Radiation Dosage, ddc:616.0757, Risk Assessment, Sensitivity and Specificity, Radiation Injuries/prevention & control, Cohort Studies, Young Adult, medicine, Image Processing, Computer-Assisted, Humans, Radiology, Nuclear Medicine and imaging, Prospective Studies, Radiation Injuries, ddc:612, Neuroradiology, Aged, Lung Neoplasms/radiography, Pulmonary Emphysema/radiography, Solitary pulmonary nodule, Analysis of Variance, Radon transform, Solitary Pulmonary Nodule/radiography, business.industry, Solitary Pulmonary Nodule, General Medicine, Radiography, Thoracic/adverse effects/methods, Middle Aged, Models, Theoretical, medicine.disease, Pulmonary Emphysema, Industrial radiography, Radiography, Thoracic, Female, Tomography, Radiology, business, Nuclear medicine, Tomography, X-Ray Computed, Tomography, X-Ray Computed/adverse effects/methods, Algorithms
Abstract

Objectives: The purpose of this study was to assess the diagnostic image quality of ultra-low-dose chest computed tomography (ULD-CT) obtained with a radiation dose comparable to chest radiography and reconstructed with filtered back projection (FBP), adaptive statistical iterative reconstruction (ASIR) and model-based iterative reconstruction (MBIR) in comparison with standard dose diagnostic CT (SDD-CT) or low-dose diagnostic CT (LDD-CT) reconstructed with FBP alone. Methods: Unenhanced chest CT images of 42 patients acquired with ULD-CT were compared with images obtained with SDD-CT or LDD-CT in the same examination. Noise measurements and image quality, based on conspicuity of chest lesions on all CT data sets were assessed on a five-point scale. Results: The radiation dose of ULD-CT was 0.16 ± 0.006mSv compared with 11.2 ± 2.7mSv for SDD-CT (P

Published
2013

37. Requirement for Innate Immunity and CD90+ NK1.1− Lymphocytes to Treat Established Melanoma with Chemo-Immunotherapy

Author

Moskalenko, Marina, primary, Pan, Michael, additional, Fu, Yichun, additional, de Moll, Ellen H., additional, Hashimoto, Daigo, additional, Mortha, Arthur, additional, Leboeuf, Marylene, additional, Jayaraman, Padmini, additional, Bernardo, Sebastian, additional, Sikora, Andrew G., additional, Wolchok, Jedd, additional, Bhardwaj, Nina, additional, Merad, Miriam, additional, and Saenger, Yvonne, additional

Published
2015
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38. CONSULTAAUTOR Blood-derived dermal langerin+ dendritic cells survey the skin in the steady state

Author

Ginhoux, Florent, Collin, Matthew P, Bogunovic, Milena, Abel, Michal, Leboeuf, Marylene, Helft, Julie, Ochando, Jordi, Kissenpfennig, Adrien, Malissen, Bernard, Grisotto, Marcos, Snoeck, Hans, Randolph, Gwendalyn, and Merad, Miriam

Subjects
integumentary system, chemical and pharmacologic phenomena, hemic and immune systems
Abstract

Langerin is a C-type lectin receptor that recognizes glycosylated patterns on pathogens. Langerin is used to identify human and mouse epidermal Langerhans cells (LCs), as well as migratory LCs in the dermis and the skin draining lymph nodes (DLNs). Using a mouse model that allows conditional ablation of langerin(+) cells in vivo, together with congenic bone marrow chimeras and parabiotic mice as tools to differentiate LC- and blood-derived dendritic cells (DCs), we have revisited the origin of langerin(+) DCs in the skin DLNs. Our results show that in contrast to the current view, langerin(+)CD8(-) DCs in the skin DLNs do not derive exclusively from migratory LCs, but also include blood-borne langerin(+) DCs that transit through the dermis before reaching the DLN. The recruitment of circulating langerin(+) DCs to the skin is dependent on endothelial selectins and CCR2, whereas their recruitment to the skin DLNs requires CCR7 and is independent of CD62L. We also show that circulating langerin(+) DCs patrol the dermis in the steady state and migrate to the skin DLNs charged with skin antigens. We propose that this is an important and previously unappreciated element of immunosurveillance that needs to be taken into account in the design of novel vaccine strategies.

Published
2007

39. Epigenetic modulation of inflammation and synaptic plasticity promotes resilience against stress in mice.

Author

Jun Wang, Hodes, Georgia E., Hongxing Zhang, Song Zhang, Wei Zhao, Golden, Sam A., Weina Bi, Menard, Caroline, Kana, Veronika, Leboeuf, Marylene, Marc Xie, Bregman, Dana, Pfau, Madeline L., Flanigan, Meghan E., Esteban-Fernández, Adelaida, Yemul, Shrishailam, Sharma, Ali, Lap Ho, Dixon, Richard, and Merad, Miriam

Subjects
NEUROPLASTICITY, MENTAL depression, EPIGENETICS, HISTONE acetylation, BRAIN abnormalities
Abstract

Major depressive disorder is associated with abnormalities in the brain and the immune system. Chronic stress in animals showed that epigenetic and inflammatory mechanisms play important roles in mediating resilience and susceptibility to depression. Here, through a highthroughput screening, we identify two phytochemicals, dihydrocaffeic acid (DHCA) and malvidin-3'-O-glucoside (Mal-gluc) that are effective in promoting resilience against stress by modulating brain synaptic plasticity and peripheral inflammation. DHCA/Mal-gluc also significantly reduces depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of hematopoietic progenitor cells from stresssusceptible mice. DHCA reduces pro-inflammatory interleukin 6 (IL-6) generations by inhibiting DNA methylation at the CpG-rich IL-6 sequences introns 1 and 3, while Mal-gluc modulates synaptic plasticity by increasing histone acetylation of the regulatory sequences of the Rac1 gene. Peripheral inflammation and synaptic maladaptation are in line with newly hypothesized clinical intervention targets for depression that are not addressed by currently available antidepressants. [ABSTRACT FROM AUTHOR]

Published
2018
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40. BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups

Author

Berres, Marie-Luise, primary, Lim, Karen Phaik Har, additional, Peters, Tricia, additional, Price, Jeremy, additional, Takizawa, Hitoshi, additional, Salmon, Hélène, additional, Idoyaga, Juliana, additional, Ruzo, Albert, additional, Lupo, Philip J., additional, Hicks, M. John, additional, Shih, Albert, additional, Simko, Stephen J., additional, Abhyankar, Harshal, additional, Chakraborty, Rikhia, additional, Leboeuf, Marylene, additional, Beltrão, Monique, additional, Lira, Sérgio A., additional, Heym, Kenneth M., additional, Clausen, Björn E., additional, Bigley, Venetia, additional, Collin, Matthew, additional, Manz, Markus G., additional, McClain, Kenneth, additional, Merad, Miriam, additional, and Allen, Carl E., additional

Published
2015
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41. Langerhans Cell Homeostasis and Turnover After Nonmyeloablative and Myeloablative Allogeneic Hematopoietic Cell Transplantation

Author

Mielcarek, Marco, primary, Kirkorian, Anna Yasmine, additional, Hackman, Robert C., additional, Price, Jeremy, additional, Storer, Barry E., additional, Wood, Brent L., additional, Leboeuf, Marylene, additional, Bogunovic, Milena, additional, Storb, Rainer, additional, Inamoto, Yoshihiro, additional, Flowers, Mary E., additional, Martin, Paul J., additional, Collin, Matthew, additional, and Merad, Miriam, additional

Published
2014
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42. Central Role of Conventional Dendritic Cells in Regulation of Bone Marrow Release and Survival of Neutrophils

Author

Jiao, Jingjing, primary, Dragomir, Ana-Cristina, additional, Kocabayoglu, Peri, additional, Rahman, Adeeb H., additional, Chow, Andrew, additional, Hashimoto, Daigo, additional, Leboeuf, Marylene, additional, Kraus, Thomas, additional, Moran, Thomas, additional, Carrasco-Avino, Gonzalo, additional, Friedman, Scott L., additional, Merad, Miriam, additional, and Aloman, Costica, additional

Published
2014
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43. BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups

Author

Berres, Marie-Luise, primary, Lim, Karen Phaik Har, additional, Peters, Tricia, additional, Price, Jeremy, additional, Takizawa, Hitoshi, additional, Salmon, Hélène, additional, Idoyaga, Juliana, additional, Ruzo, Albert, additional, Lupo, Philip J., additional, Hicks, M. John, additional, Shih, Albert, additional, Simko, Stephen J., additional, Abhyankar, Harshal, additional, Chakraborty, Rikhia, additional, Leboeuf, Marylene, additional, Beltrão, Monique, additional, Lira, Sérgio A., additional, Heym, Kenneth M., additional, Clausen, Björn E., additional, Bigley, Venetia, additional, Collin, Matthew, additional, Manz, Markus G., additional, McClain, Kenneth, additional, Merad, Miriam, additional, and Allen, Carl E., additional

Published
2014
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44. Abstract A43: Therapeutic efficacy of antitumor monoclonal antibodies combined with chemotherapy depends on innate immunity and NK1.1- innate lymphoid cells.

Author

Moskalenko, Marina, primary, Pan, Michael, additional, Hashimoto, Daigo, additional, Mortha, Arthur, additional, Bernardo, Sebastian G., additional, Leboeuf, Marylene, additional, Houghton, Alan, additional, Wolchok, Jedd, additional, Burakoff, Steven, additional, Merad, Miriam, additional, and Saenger, Yvonne M., additional

Published
2013
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45. CD169+ Macrophages Regulate Erythropoiesis Under Homeostasis, Recovery From Erythron Injury and in JAK2V617F-Induced Polycythemia Vera

Author

Chow, Andrew, primary, Huggins, Matthew, additional, Ahmed, Jalal, additional, Lucas, Daniel, additional, Hashimoto, Daigo, additional, Kunisaki, Yuya, additional, Pinho, Sandra, additional, Leboeuf, Marylene, additional, Noizat, Clara, additional, van Rooijen, Nico, additional, Tanaka, Masato, additional, Zhao, Zhizhuang Joe, additional, Bergman, Aviv, additional, Merad, Miriam, additional, and Frenette, Paul S., additional

Published
2012
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46. Systemic Analysis of PPARγ in Mouse Macrophage Populations Reveals Marked Diversity in Expression with Critical Roles in Resolution of Inflammation and Airway Immunity

Author

Gautier, Emmanuel L., primary, Chow, Andrew, additional, Spanbroek, Rainer, additional, Marcelin, Genevieve, additional, Greter, Melanie, additional, Jakubzick, Claudia, additional, Bogunovic, Milena, additional, Leboeuf, Marylene, additional, van Rooijen, Nico, additional, Habenicht, Andreas J., additional, Merad, Miriam, additional, and Randolph, Gwendalyn J., additional

Published
2012
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47. RAF/MEK/extracellular signal–related kinase pathway suppresses dendritic cell migration and traps dendritic cells in Langerhans cell histiocytosis lesions

Author

Hogstad, Brandon, Berres, Marie-Luise, Chakraborty, Rikhia, Tang, Jun, Bigenwald, Camille, Serasinghe, Madhavika, Lim, Karen Phaik Har, Lin, Howard, Man, Tsz-Kwong, Remark, Romain, Baxter, Samantha, Kana, Veronika, Jordan, Stefan, Karoulia, Zoi, Kwan, Wing-hong, Leboeuf, Marylene, Brandt, Elisa, Salmon, Helene, McClain, Kenneth, Poulikakos, Poulikos, Chipuk, Jerry, Mulder, Willem J.M., Allen, Carl E., and Merad, Miriam

Abstract

Langerhans cell histiocytosis (LCH) is an inflammatory myeloid neoplasia characterized by granulomatous lesions containing pathological CD207+ dendritic cells (DCs) with constitutively activated mitogen-activated protein kinase (MAPK) pathway signaling. Approximately 60% of LCH patients harbor somatic BRAFV600E mutations localizing to CD207+ DCs within lesions. However, the mechanisms driving BRAFV600E+ LCH cell accumulation in lesions remain unknown. Here we show that sustained extracellular signal–related kinase activity induced by BRAFV600E inhibits C-C motif chemokine receptor 7 (CCR7)–mediated DC migration, trapping DCs in tissue lesions. Additionally, BRAFV600E increases expression of BCL2-like protein 1 (BCL2L1) in DCs, resulting in resistance to apoptosis. Pharmacological MAPK inhibition restores migration and apoptosis potential in a mouse LCH model, as well as in primary human LCH cells. We also demonstrate that MEK inhibitor-loaded nanoparticles have the capacity to concentrate drug delivery to phagocytic cells, significantly reducing off-target toxicity. Collectively, our results indicate that MAPK tightly suppresses DC migration and augments DC survival, rendering DCs in LCH lesions trapped and resistant to cell death.

Published
2018
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48. Pretransplant CSF-1 therapy expands recipient macrophages and ameliorates GVHD after allogeneic hematopoietic cell transplantation

Author

Hashimoto, Daigo, primary, Chow, Andrew, additional, Greter, Melanie, additional, Saenger, Yvonne, additional, Kwan, Wing-Hong, additional, Leboeuf, Marylene, additional, Ginhoux, Florent, additional, Ochando, Jordi C., additional, Kunisaki, Yuya, additional, van Rooijen, Nico, additional, Liu, Chen, additional, Teshima, Takanori, additional, Heeger, Peter S., additional, Stanley, E. Richard, additional, Frenette, Paul S., additional, and Merad, Miriam, additional

Published
2011
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49. Bone marrow CD169+ macrophages promote the retention of hematopoietic stem and progenitor cells in the mesenchymal stem cell niche

Author

Chow, Andrew, primary, Lucas, Daniel, additional, Hidalgo, Andrés, additional, Méndez-Ferrer, Simón, additional, Hashimoto, Daigo, additional, Scheiermann, Christoph, additional, Battista, Michela, additional, Leboeuf, Marylene, additional, Prophete, Colette, additional, van Rooijen, Nico, additional, Tanaka, Masato, additional, Merad, Miriam, additional, and Frenette, Paul S., additional

Published
2011
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