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427 results on '"Gysemans, Conny A."'

1. List of contributors

Author

Adams, John S., primary, Amrein, Karin, additional, Anderson, Paul H., additional, Arnold, Leggy A., additional, Arora, Juhi, additional, Artusa, Patricio, additional, Ascherio, Alberto, additional, Asmussen, Niels C., additional, Astier, Anne L., additional, Bak, Min Ji, additional, Bauerle, Kevin T., additional, Belorusova, Anna Y., additional, Benkusky, Nancy A., additional, Bernal-Mizrachi, Carlos, additional, Bhattoa, Harjit P., additional, Bikle, Daniel D., additional, Bilezikian, John P., additional, Binkley, Neil C., additional, Bischoff-Ferrari, Heike A., additional, Bishop, Charles W., additional, Blomberg Jensen, Martin, additional, Boisen, Ida Marie, additional, Boucher, Barbara J., additional, Bouillon, Roger, additional, Boyan, Barbara D., additional, Bradford, Dana, additional, Brancatella, Alessandro, additional, Buburuzan, Laura, additional, Burne, Thomas H.J., additional, Buschittari, Damien, additional, Calkins, Hannah, additional, Calvo, Mona S., additional, Camargo, Carlos A., additional, Campbell, Moray J., additional, Cantorna, Margherita T., additional, Cappellani, Daniele, additional, Carlberg, Carsten, additional, Carmeliet, Geert, additional, Cashman, Kevin D., additional, Ceglia, Lisa, additional, Cetani, Filomena, additional, Chang, Wenhan, additional, Cheadle, Charlotte, additional, Chou, Sharon H., additional, Christakos, Sylvia, additional, Christopher, Kenneth B., additional, Chu, Emily Y., additional, Chun, Rene F., additional, Cleal, Jane K., additional, Cobice, Diego F., additional, Cooper, Cyrus, additional, Coort, Susan L.M., additional, Cui, Xiaoying, additional, Curtis, Elizabeth M., additional, Danilenko, Michael, additional, Darling, Andrea L., additional, David Roodman, G., additional, Dawson-Hughes, Bess, additional, de Jongh, Renate, additional, Demay, Marie B., additional, Dennison, Elaine M., additional, Dixon, Katie M., additional, Dong, Bingning, additional, Doroudi, Maryam, additional, Dusso, Adriana, additional, Dvorzhinskiy, Aleksey, additional, Ebeling, Peter R., additional, Erben, Reinhold G., additional, Evelo, Chris T.A., additional, Eyles, Darryl, additional, Feldman, David, additional, Ferrer-Mayorga, Gemma, additional, Fleet, James C., additional, Forcellati, Marianela, additional, Foster, Brian L., additional, Gafni, Rachel I., additional, Gayan-Ramirez, Ghislaine, additional, Giovannucci, Edward, additional, Girgis, Christian M., additional, Glencross, Drew A., additional, Glorieux, Francis H., additional, Gocek, Elzbieta, additional, Goldfarb, David S., additional, Goltzman, David, additional, González-Sancho, José Manuel, additional, Grant, William B., additional, Groves, Natalie J., additional, Gysemans, Conny, additional, Harrison, Stephanie, additional, Harvey, Nicholas C., additional, Haseltine, Katherine, additional, Hawrylowicz, Catherine M., additional, Hayes, Colleen E., additional, Heckel, John E., additional, Hershberger, Pamela A., additional, Hewison, Martin, additional, Högler, Wolfgang, additional, Holick, Michael F., additional, Hollis, Bruce W., additional, Holt, Rune, additional, Hujoel, Philippe P., additional, Hyppönen, Elina, additional, Ismailova, Aiten, additional, Jablonski, Nina G., additional, Jakobsen, Jette, additional, Janssens, Wim, additional, Jeffery, Louisa, additional, Jenkinson, Carl, additional, Jensen, Marie Bagge, additional, Jetten, Anton M., additional, Jiang, Heng, additional, Johnson, Candace S., additional, Jones, Glenville, additional, Jones, Kerry S., additional, Jüppner, Harald, additional, Kalia, Vandana, additional, Kallay, Enikö, additional, Karapalis, Andrew C., additional, Kaufmann, Martin, additional, Kiely, Mairead, additional, Kim, Hanseul, additional, Kim, Tiffany Y., additional, Kojima, Hiroyuki, additional, Kooij, Ireen, additional, Kovacs, Christopher S., additional, Kremer, Richard, additional, Krieger, Kirsten, additional, Kritmetapak, Kittrawee, additional, Krueger, Diane C., additional, Kumar, Rajiv, additional, Kurihara, Noriyoshi, additional, Lane, Joseph M., additional, Lanham-New, Susan A., additional, Latic, Nejla, additional, LeBoff, Meryl S., additional, Lee, Maija B., additional, Lee, Seong Min, additional, Levine, Michael A., additional, Lewis, Richard, additional, Lewis, Rohan M., additional, Li, Wei, additional, Li, Yan Chun, additional, Lincoln, Matthew R., additional, Lips, Paul, additional, Lisse, Thomas S., additional, Liu, Eva S., additional, López de Maturana, Evangelina, additional, Lugg, Sebastian T., additional, Machado, Christopher J., additional, Maes, Karen, additional, Maestro, Miguel A., additional, Malats, Núria, additional, Malloy, Peter J., additional, Manousaki, Despoina, additional, Marcinkowska, Ewa, additional, Marcocci, Claudio, additional, Martens, Pieter-Jan, additional, Martineau, Adrian R., additional, Mason, Rebecca S., additional, Mathieu, Chantal, additional, Mayne, Phoebe, additional, McGrath, John J., additional, Mehta, Mansi, additional, Mellanby, Richard John, additional, Merchant, Nadia, additional, Meyer, Mark B., additional, Miao, Dengshun, additional, Moon, Rebecca J., additional, Mortensen, Li Juel, additional, Motlaghzadeh, Yasaman, additional, Munger, Kassandra L., additional, Muñoz, Alberto, additional, Nakamichi, Yuko, additional, Narvaez, Carmen J., additional, Nikiphorou, Elena, additional, Nonn, Larisa, additional, Pal, Lubna, additional, Parekh, Dhruv, additional, Pettifor, John M., additional, Pike, J. Wesley, additional, Pilz, Stefan, additional, Pittas, Anastassios G., additional, Pludowski, Pawel, additional, Prosser, David E., additional, Pullagura, Sri Ramulu N., additional, Raphael, Joseph, additional, Rauz, Saaeha, additional, Raza, Karim, additional, Real, Francisco X., additional, Reichrath, Jörg, additional, Richards, J. Brent, additional, Rivadeneira, Fernando, additional, Rochel, Natacha, additional, Roizen, Jeffrey D., additional, Ryan, Brittany A., additional, Sarkar, Surojit, additional, Sarmadi, Fatemeh, additional, Schafer, Anne L., additional, Schepelmann, Martin, additional, Schoenmakers, Inez, additional, Schuit, Frans, additional, Schwartz, Zvi, additional, Scott, Kayla M., additional, Sellmeyer, Deborah E., additional, Sempos, Christopher T., additional, Sepiashvili, Lusia, additional, Seshadri, Mukund, additional, Shane, Elizabeth, additional, Shaurova, Tatiana, additional, Shieh, Albert, additional, Shui, Irene, additional, Singh, Ravinder J., additional, Slominski, Andrzej T., additional, Smith, Karl W., additional, St-Arnaud, René, additional, Stein, Emily M., additional, Studzinski, George P., additional, Suda, Tatsuo, additional, Takahashi, Naoyuki, additional, Taylor, Hugh S., additional, Tebben, Peter J., additional, Thacher, Tom D., additional, Thandrayen, Kebashni, additional, Thickett, David R., additional, Tiosano, Dov, additional, Trajanoska, Katerina, additional, Tu, Chia-Ling, additional, Tuckey, Robert C., additional, Tutaworn, Teerapat, additional, Udagawa, Nobuyuki, additional, Uday, Suma, additional, Unnanuntana, Aasis, additional, van Driel, Marjolein, additional, van Leeuwen, Johannes P.T.M., additional, van Schoor, Natasja, additional, Verlinden, Lieve, additional, Vieth, Reinhold, additional, Vimaleswaran, Karina S., additional, Wagner, Carol L., additional, Wallace, Graham R., additional, Weaver, Connie M., additional, Webb, Daniel A., additional, Welsh, JoEllen, additional, White, John H., additional, Whiting, Susan J., additional, Williams, Emma L., additional, Yahyavi, Sam Kafai, additional, Yamamoto, Keiko, additional, Yates, Clayton, additional, Zagorac, Sladjana, additional, Zhang, Rong Mei, additional, Zhao, Hengguang, additional, Zhou, Ang, additional, and Zittermann, Armin, additional

Published
2024
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5. Single-cell profiling of myeloid cells in glioblastoma across species and disease stage reveals macrophage competition and specialization

Author

Pombo Antunes, Ana Rita, Scheyltjens, Isabelle, Lodi, Francesca, Messiaen, Julie, Antoranz, Asier, Duerinck, Johnny, Kancheva, Daliya, Martens, Liesbet, De Vlaminck, Karen, Van Hove, Hannah, Kjølner Hansen, Signe Schmidt, Bosisio, Francesca Maria, Van der Borght, Koen, De Vleeschouwer, Steven, Sciot, Raf, Bouwens, Luc, Verfaillie, Michiel, Vandamme, Niels, Vandenbroucke, Roosmarijn E., De Wever, Olivier, Saeys, Yvan, Guilliams, Martin, Gysemans, Conny, Neyns, Bart, De Smet, Frederik, Lambrechts, Diether, Van Ginderachter, Jo A., and Movahedi, Kiavash

Published
2021
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10. A plasma miR-193b-365 signature combined with age and glycemic status predicts response to Lactococcus lactis-based antigen-specific immunotherapy in new-onset type 1 diabetes

Author

Sassi, Gabriele, primary, Licata, Giada, primary, Ventriglia, Giuliana, primary, Wouters, Amber, primary, Lemaitre, Pierre, primary, Seurinck, Ruth, primary, Mori, Alessia, primary, Emanuela Grieco, Giuseppina, primary, Bissenova, Samal, primary, Ellis, Darcy, primary, Caluwaerts, Silvia, primary, Rottiers, Pieter, primary, Vandamme, Niels, primary, Mathieu, Chantal, primary, Dotta, Francesco, primary, Gysemans, Conny, primary, and Sebastiani, Guido, primary

Published
2023
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14. High-Throughput Analysis of Neutrophil Extracellular Trap Levels in Subtypes of People with Type 1 Diabetes

Author

Bissenova, Samal, Buitinga, Mijke, Boesch, Markus, Korf, Hannelie, Casteels, Kristina, Teunkens, An, Mathieu, Chantal, and Gysemans, Conny

Abstract

Neutrophils might play an important role in the pathogenesis of autoimmune diseases, including type 1 diabetes (T1D), by contributing to immune dysregulation via a highly inflammatory program called neutrophil extracellular trap (NET) formation or NETosis, involving the extrusion of chromatin entangled with anti-microbial proteins. However, numerous studies reported contradictory data on NET formation in T1D. This might in part be due to the inherent heterogeneity of the disease and the influence of the disease developmental stage on neutrophil behavior. Moreover, there is a lack of a standardized method to measure NETosis in an unbiased and robust manner. In this study, we employed the Incucyte® ZOOM live-cell imaging platform to study NETosis levels in various subtypes of adult and pediatric T1D donors compared to healthy controls (HC) at baseline and in response to phorbol-myristate acetate (PMA) and ionomycin. Firstly, we determined that the technique allows for an operator-independent and automated quantification of NET formation across multiple time points, which showed that PMA and ionomycin induced NETosis with distinct kinetic characteristics, confirmed by high-resolution microscopy. NETosis levels also showed a clear dose-response curve to increasing concentrations of both stimuli. Overall, using Incucyte® ZOOM, no aberrant NET formation was observed over time in the different subtypes of T1D populations, irrespective of age, compared to HC. These data were corroborated by the levels of peripheral NET markers in all study participants. The current study showed that live-cell imaging allows for a robust and unbiased analysis and quantification of NET formation in real-time. Peripheral neutrophil measures should be complemented with dynamic quantification of NETing neutrophils to make robust conclusions on NET formation in health and disease. ispartof: BIOLOGY-BASEL vol:12 issue:6 ispartof: location:Switzerland status: published

Published
2023

15. List of Contributors

Author

Adams, John S., primary, Adams, Judith E., additional, Alsalem, Jawaher A., additional, Anderson, Paul H., additional, Andreopoulou, Panagiota, additional, Angellotti, Edith, additional, Arnold, Leggy A., additional, Atkins, Gerald J., additional, Barbáchano, Antonio, additional, Bassuk, Shari S., additional, Beaudin, Sarah, additional, Belorusova, Anna Y., additional, Benkusky, Nancy A., additional, Bernal-Mizrachi, Carlos, additional, Bhan, Ishir, additional, Bhattoa, Harjit P., additional, Bikle, Daniel D., additional, Bilezikian, John P., additional, Binkley, Neil C., additional, Bischoff-Ferrari, Heike A., additional, Bishop, Charles W., additional, Boisen, Ida M., additional, Bonelli, Fabrizio, additional, Boskey, Adele L., additional, Boucher, Barbara J., additional, Bouillon, Roger, additional, Bouttier, Manuella, additional, Boyan, Barbara D., additional, Bruce, Danny, additional, Buburuzan, Laura, additional, Burghardt, Andrew J., additional, Burne, Thomas H.J., additional, Calvo, Mona S., additional, Camargo Jr., Carlos A., additional, Cannata-Andia, Jorge B., additional, Cantorna, Margherita T., additional, Carlberg, Carsten, additional, Carmeliet, Geert, additional, Carpenter, Thomas O., additional, Carter, Graham D., additional, Cashman, Kevin D., additional, Ceglia, Lisa, additional, Christakos, Sylvia, additional, Christopher, Kenneth B., additional, Chun, Rene F., additional, Coe, Fredric L., additional, Coffman, Frederick, additional, Compston, Juliet, additional, Cooper, Cyrus, additional, Curtis, Elizabeth M., additional, Cusano, Natalie E., additional, Danilenko, Michael, additional, David Roodman, G., additional, Dawson-Hughes, Bess, additional, De Clercq, Pierre, additional, DeLuca, Hector F., additional, Demaret, Julie, additional, Demay, Marie B., additional, Dempster, David W., additional, Dennison, Elaine M., additional, Dhawan, Puneet, additional, Dimitrov, Vassil, additional, Dixon, Katie M., additional, Doroudi, Maryam, additional, Doyle, Shevaun M., additional, Dusso, Adriana S., additional, Dvorzhinskiy, Aleksey, additional, Ebeling, Peter R., additional, Eisman, John A., additional, Emkey, Gregory R., additional, Epstein Jr., Ervin H., additional, Epstein, Sol, additional, Eyles, Darryl, additional, Favus, Murray J., additional, Feldman, David, additional, Ferrer-Mayorga, Gemma, additional, Findlay, David M., additional, Fleet, James C., additional, Foster, Brian L., additional, Franceschi, Renny T., additional, Fraser, David R., additional, Furst, Jessica M., additional, Gafni, Rachel I., additional, Giovannucci, Edward, additional, Girgis, Christian M., additional, Gleason, James L., additional, Glorieux, Francis H., additional, Gocek, Elzbieta, additional, Goltzman, David, additional, González-Sancho, José Manuel, additional, Graeff-Armas, Laura A., additional, Grant, William B., additional, Groves, Natalie J., additional, Gysemans, Conny, additional, Hansen, Lasse Bøllehuus, additional, Harvey, Nicholas C., additional, Hawrylowicz, Catherine M., additional, Hayes, Colleen E., additional, Heaney, Robert P., additional, Hendy, Geoffrey N., additional, Hershberger, Pamela A., additional, Hewison, Martin, additional, Holick, Michael F., additional, Hollis, Bruce W., additional, Hujoel, Philippe P., additional, Hyppönen, Elina, additional, Insogna, Karl L., additional, Jablonski, Nina G., additional, Jensen, Martin Blomberg, additional, Jolliffe, David A., additional, Jones, Glenville, additional, Jones, Kerry S., additional, Jüppner, Harald, additional, Kallay, Enikö, additional, Karaplis, Andrew C., additional, Kaufmann, Martin, additional, Kiely, Mairead, additional, Kim, Tiffany Y., additional, Konrad, Martin, additional, Kovacs, Christopher S., additional, Kremer, Richard, additional, Krug, Roland, additional, Kumar, Rajiv, additional, Kurihara, Noriyoshi, additional, Laing, Emma, additional, Lane, Joseph M., additional, Larner, Dean P., additional, Larriba, María Jesús, additional, Laverny, Gilles, additional, Le Roy, Nathalie, additional, Lee, Seong M., additional, Levine, Michael A., additional, Lewis, Richard, additional, Lips, Paul, additional, Lisse, Thomas S., additional, Liu, Eva S., additional, Liu, Philip T., additional, Li, Yan, additional, Li, Yan Chun, additional, MacKrell, James G., additional, Mady, Leila J., additional, Majumdar, Sharmila, additional, Makishima, Makoto, additional, Malloy, Peter J., additional, Mann, Elizabeth H., additional, Manson, JoAnn E., additional, Martineau, Adrian R., additional, Mason, Rebecca S., additional, Mathieu, Chantal, additional, Matsumoto, Toshio, additional, Matthews, Donald G., additional, McGrath, John J., additional, Metzger, Daniel, additional, Meyer, Mark B., additional, Miao, Denshun, additional, Mizwicki, Mathew T., additional, Moon, Rebecca J., additional, Morris, Howard A., additional, Mortensen, Li J., additional, Muñoz, Alberto, additional, Nakamichi, Yuko, additional, Narvaez, Carmen J., additional, Nashold, Faye E., additional, Naveh-Many, Tally, additional, Nielson, Carrie M., additional, Norman, Anthony W., additional, Nys, Yves, additional, Onal, Melda, additional, Pal, Lubna, additional, Patterson, Kristine Y., additional, Pauwels, Steven, additional, Pehrsson, Pamela R., additional, Petkovich, Martin, additional, Pettifor, John M., additional, Pfeffer, Paul E., additional, Phillips, Katherine M., additional, Pike, J. Wesley, additional, Pilz, Stefan, additional, Pittas, Anastassios G., additional, Pludowski, Pawel, additional, Prosser, David E., additional, Pullagura, Sri Ramulu N., additional, Quarles, L. Darryl, additional, Rajagopal, Rithwick, additional, Ransohoff, Katherine J., additional, Rauz, Saaeha, additional, Rebolledo, Brian J., additional, Reichrath, Jörg, additional, Rieger, Sandra, additional, Riek, Amy E., additional, Rochel, Natacha, additional, Roizen, Jeffrey D., additional, Roseland, Janet M., additional, Rosen, Cliff, additional, Rybchyn, Mark S., additional, Saitoh, Hiroshi, additional, Salehi-Tabar, Reyhaneh, additional, Schafer, Anne L., additional, Schlingmann, Karl P., additional, Schoenmakers, Inez, additional, Schwartz, Zvi, additional, Scott, Kayla, additional, Sempos, Christopher T., additional, Sepiashvili, Lusia, additional, Seshadri, Mukund, additional, Shane, Elizabeth, additional, Shaurova, Tatiana, additional, Shui, Irene, additional, Silver, Justin, additional, Singh, Ravinder J., additional, Skingle, Linda, additional, St-Arnaud, René, additional, Starr, Jessica, additional, Stayrook, Keith R., additional, Stein, Emily M., additional, Stites, Ryan E., additional, Studzinski, George P., additional, Suda, Tatsuo, additional, Takahashi, Fumiaki, additional, Takahashi, Naoyuki, additional, Tang, Jean Y., additional, Taylor, Christine L., additional, Taylor, Hugh S., additional, Tebben, Peter J., additional, Thacher, Thomas D., additional, Thadhani, Ravi, additional, Thandrayen, Kebashni, additional, Thys-Jacobs, Susan, additional, Tiosano, Dov, additional, Toni, Roberto, additional, Towler, Dwight A., additional, Trump, Donald L., additional, Udagawa, Nobuyuki, additional, Uitterlinden, André G., additional, Unnanuntana, Aasis, additional, van de Peppel, Jeroen, additional, van der Eerden, Bram C.J., additional, van Driel, Marjolein, additional, van Leeuwen, Johannes P.T.M., additional, van Schoor, Natasja, additional, Vanherwegen, An-Sofie, additional, Vazirnia, Aria, additional, Verlinden, Lieve, additional, Verstuyf, Annemieke, additional, Vieth, Reinhold, additional, Wagner, Carol L., additional, Wallace, Graham R., additional, Weaver, Connie, additional, Welsh, JoEllen, additional, White, John H., additional, Whiting, Susan J., additional, Whyte, Michael P., additional, Wysolmerski, John J., additional, Yamada, Sachiko, additional, Yu, Olivia B., additional, Zavala, Kathryn, additional, Zechner, Christoph, additional, Zeytinoglu, Meltem, additional, and Zhao, Hengguang, additional

Published
2018
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18. A Plasma miR-193b-365 Signature Combined With Age and Glycemic Status Predicts Response to Lactococcus lactis–Based Antigen-Specific Immunotherapy in New-Onset Type 1 Diabetes.

Author

Sassi, Gabriele, Licata, Giada, Ventriglia, Giuliana, Wouters, Amber, Lemaitre, Pierre, Seurinck, Ruth, Mori, Alessia, Grieco, Giuseppina Emanuela, Bissenova, Samal, Ellis, Darcy, Caluwaerts, Silvia, Rottiers, Pieter, Vandamme, Niels, Mathieu, Chantal, Dotta, Francesco, Gysemans, Conny, and Sebastiani, Guido

Subjects
TYPE 1 diabetes, LACTOCOCCUS, LACTOCOCCUS lactis, PROGNOSIS, PATIENT selection, PANCREATIC tumors, HYPERGLYCEMIA
Abstract

Immunomodulation combined with antigen therapy holds great promise to arrest autoimmune type 1 diabetes, but clinical translation is hampered by a lack of prognostic biomarkers. Low-dose anti-CD3 plus Lactococcus lactis bacteria secreting proinsulin and IL-10 reversed new-onset disease in nonobese diabetic (NOD) mice, yet some mice were resistant to the therapy. Using miRNA profiling, six miRNAs (i.e., miR-34a-5p, miR-125a-3p, miR-193b-3p, miR-328, miR-365–3p, and miR-671–3p) were identified as differentially expressed in plasma of responder versus nonresponder mice before study entry. After validation and stratification in an independent cohort, plasma miR-193b-3p and miR-365–3p, combined with age and glycemic status at study entry, had the best power to predict, with high sensitivity and specificity, poor response to the therapy. These miRNAs were highly abundant in pancreas-infiltrating neutrophils and basophils with a proinflammatory and activated phenotype. Here, a set of miRNAs and disease-associated parameters are presented as a predictive signature for the L. lactis–based immunotherapy outcome in new-onset type 1 diabetes, hence allowing targeted recruitment of trial participants and accelerated trial execution. Article Highlights: Low-dose anti-CD3 combined with oral gavage of genetically modified Lactococcus lactis bacteria secreting human proinsulin and IL-10 holds great promise to arrest autoimmune type 1 diabetes, but the absence of biomarkers predicting therapeutic success hampers clinical translation. A set of cell-free circulation miRNAs together with age and glycemia at baseline predicts a poor response after L. lactis–based immunotherapy in nonobese mice with new-onset diabetes. Pancreas-infiltrating neutrophils and basophils are identified as potential cellular sources of discovered miRNAs. The prognostic signature could guide targeted recruitment of patients with newly diagnosed type 1 diabetes in clinical trials with the L. lactis–based immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Supplementary Figures 1 through 5 from Tumor Hypoxia Does Not Drive Differentiation of Tumor-Associated Macrophages but Rather Fine-Tunes the M2-like Macrophage Population

Author

Laoui, Damya, primary, Van Overmeire, Eva, primary, Di Conza, Giusy, primary, Aldeni, Chiara, primary, Keirsse, Jiri, primary, Morias, Yannick, primary, Movahedi, Kiavash, primary, Houbracken, Isabelle, primary, Schouppe, Elio, primary, Elkrim, Yvon, primary, Karroum, Oussama, primary, Jordan, Bénédicte, primary, Carmeliet, Peter, primary, Gysemans, Conny, primary, De Baetselier, Patrick, primary, Mazzone, Massimiliano, primary, and Van Ginderachter, Jo A., primary

Published
2023
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20. Data from Tumor Hypoxia Does Not Drive Differentiation of Tumor-Associated Macrophages but Rather Fine-Tunes the M2-like Macrophage Population

Author

Laoui, Damya, primary, Van Overmeire, Eva, primary, Di Conza, Giusy, primary, Aldeni, Chiara, primary, Keirsse, Jiri, primary, Morias, Yannick, primary, Movahedi, Kiavash, primary, Houbracken, Isabelle, primary, Schouppe, Elio, primary, Elkrim, Yvon, primary, Karroum, Oussama, primary, Jordan, Bénédicte, primary, Carmeliet, Peter, primary, Gysemans, Conny, primary, De Baetselier, Patrick, primary, Mazzone, Massimiliano, primary, and Van Ginderachter, Jo A., primary

Published
2023
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22. Supplementary Tables 1 and 2 from Tumor Hypoxia Does Not Drive Differentiation of Tumor-Associated Macrophages but Rather Fine-Tunes the M2-like Macrophage Population

Author

Laoui, Damya, primary, Van Overmeire, Eva, primary, Di Conza, Giusy, primary, Aldeni, Chiara, primary, Keirsse, Jiri, primary, Morias, Yannick, primary, Movahedi, Kiavash, primary, Houbracken, Isabelle, primary, Schouppe, Elio, primary, Elkrim, Yvon, primary, Karroum, Oussama, primary, Jordan, Bénédicte, primary, Carmeliet, Peter, primary, Gysemans, Conny, primary, De Baetselier, Patrick, primary, Mazzone, Massimiliano, primary, and Van Ginderachter, Jo A., primary

Published
2023
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23. Supplementary Materials, Tables 1-4, Figures 1-10 from Different Tumor Microenvironments Contain Functionally Distinct Subsets of Macrophages Derived from Ly6C(high) Monocytes

Author

Movahedi, Kiavash, primary, Laoui, Damya, primary, Gysemans, Conny, primary, Baeten, Martijn, primary, Stangé, Geert, primary, Van den Bossche, Jan, primary, Mack, Matthias, primary, Pipeleers, Daniel, primary, In't Veld, Peter, primary, De Baetselier, Patrick, primary, and Van Ginderachter, Jo A., primary

Published
2023
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24. Supplementary Methods from Tumor Hypoxia Does Not Drive Differentiation of Tumor-Associated Macrophages but Rather Fine-Tunes the M2-like Macrophage Population

Author

Laoui, Damya, primary, Van Overmeire, Eva, primary, Di Conza, Giusy, primary, Aldeni, Chiara, primary, Keirsse, Jiri, primary, Morias, Yannick, primary, Movahedi, Kiavash, primary, Houbracken, Isabelle, primary, Schouppe, Elio, primary, Elkrim, Yvon, primary, Karroum, Oussama, primary, Jordan, Bénédicte, primary, Carmeliet, Peter, primary, Gysemans, Conny, primary, De Baetselier, Patrick, primary, Mazzone, Massimiliano, primary, and Van Ginderachter, Jo A., primary

Published
2023
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32. Lysine deacetylase inhibition prevents diabetes by chromatin-independent immunoregulation and β-cell protection

Author

Christensen, Dan Ploug, Gysemans, Conny, Lundh, Morten, Dahllöf, Mattias Salling, Noesgaard, Daniel, Schmidt, Søren Fisker, Mandrup, Susanne, Birkbak, Nikolai, Workmand, Christopher T., Piemonti, Lorenzo, Blaabjerg, Lykke, Monzani, Valmen, Fossati, Gianluca, Mascagni, Paolo, Paraskevas, Steven, Aikin, Reid A., Billestrup, Nils, Grunnet, Lars Groth, Dinarello, Charles A., Mathieu, Chantal, and Mandrup-Poulsen, Thomas

Published
2014

35. PTPN2 Regulates the Interferon Signaling and Endoplasmic Reticulum Stress Response in Pancreatic β-Cells in Autoimmune Diabetes

Author

Elvira, Bernat, Vandenbempt, Valerie, Bauzá-Martinez, Julia, Crutzen, Raphaël, Negueruela, Javier, Ibrahim, Hazem, Winder, Matthew L., Brahma, Manoja K., Vekeriotaite, Beata, Martens, Pieter Jan, Singh, Sumeet Pal, Rossello, Fernando, Lybaert, Pascale, Otonkoski, Timo, Gysemans, Conny, Wu, Wei, Gurzov, Esteban N., Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Afd Biomol.Mass Spect. and Proteomics, and Biomolecular Mass Spectrometry and Proteomics

Subjects
Protein Tyrosine Phosphatase, Non-Receptor Type 2, Protein Tyrosine Phosphatase, Non-Receptor Type 2/genetics, Endocrinology, Diabetes and Metabolism, Apoptosis, Type 1/metabolism, Interferon-gamma/pharmacology, Endoplasmic Reticulum Stress/physiology, Endoplasmic Reticulum Stress, Non-Receptor Type 2/genetics, Diabetes and Metabolism, Interferon-gamma, Mice, Diabetes Mellitus, Type 1, Endocrinology, Insulin-Secreting Cells/metabolism, Mice, Inbred NOD, Insulin-Secreting Cells, Apoptosis/genetics, Diabetes Mellitus, Internal Medicine, Inbred NOD, Animals, Diabetes Mellitus, Type 1/metabolism, Humans, Protein Tyrosine Phosphatase
Abstract

Type 1 diabetes (T1D) results from autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell dysfunction. Here, we assessed the global protein and individual PTP profiles in the pancreas from early onset non-obese diabetic (NOD) mice treated with an anti-CD3 monoclonal antibody and interleukin-1 receptor antagonist. The treatment reversed hyperglycemia and we observed enhanced expression of PTPN2, a PTP family member and T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the pancreatic islets. To address the functional role of PTPN2 in β-cells, we generated PTPN2-deficient human stem cell-derived β-like and EndoC-βH1 cells. Mechanistically, we demonstrated that PTPN2 inactivation in β-cells exacerbates type I and type II interferon signaling networks and the potential progression towards autoimmunity. Moreover, we established the capacity of PTPN2 to positively modulate the Ca2+-dependent unfolded protein response and ER stress outcome in β-cells. Adenovirus-induced overexpression of PTPN2 partially protected from ER-stress induced β-cell death. Our results postulate PTPN2 as a key protective factor in β-cells during inflammation and ER stress in autoimmune diabetes.

Published
2022

36. Effects of repeated infections with non-typeable Haemophilus influenzae on lung in vitamin D deficient and smoking mice.

Author

UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Centre de l'allergie, UCL - (SLuc) Service de pneumologie, Serré, Jef, Tanjeko, Ajime Tom, Mathyssen, Carolien, Heigl, Tobias, Sacreas, Annelore, Cook, Dana Paulina, Verbeken, Erik, Maes, Karen, Verhaegen, Jan, Pilette, Charles, Vanoirbeek, Jeroen, Gysemans, Conny, Mathieu, Chantal, Vanaudenaerde, Bart, Janssens, Wim, Gayan-Ramirez, Ghislaine, UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Centre de l'allergie, UCL - (SLuc) Service de pneumologie, Serré, Jef, Tanjeko, Ajime Tom, Mathyssen, Carolien, Heigl, Tobias, Sacreas, Annelore, Cook, Dana Paulina, Verbeken, Erik, Maes, Karen, Verhaegen, Jan, Pilette, Charles, Vanoirbeek, Jeroen, Gysemans, Conny, Mathieu, Chantal, Vanaudenaerde, Bart, Janssens, Wim, and Gayan-Ramirez, Ghislaine

Abstract

In chronic obstructive pulmonary disease (COPD), exacerbations cause acute inflammatory flare-ups and increase the risk for hospitalization and mortality. Exacerbations are common in all disease stages and are often caused by bacterial infections e.g., non-typeable Heamophilus influenzae (NTHi). Accumulating evidence also associates vitamin D deficiency with the severity of COPD and exacerbation frequency. However, it is still unclear whether vitamin D deficiency when combined with cigarette smoking would worsen and prolong exacerbations caused by repeated infections with the same bacterial strain. Vitamin D sufficient (VDS) and deficient (VDD) mice were exposed to nose-only cigarette smoke (CS) for 14 weeks and oropharyngeally instilled with NTHi at week 6, 10 and 14. Three days after the last instillation, mice were assessed for lung function, tissue remodeling, inflammation and immunity. The impact of VDD and CS on inflammatory cells and immunoglobulin (Ig) production was also assessed in non-infected animals while serum Ig production against NTHi and dsDNA was measured in COPD patients before and 1 year after supplementation with Vitamin D3. VDD enhanced NTHi eradication, independently of CS and complete eradication was reflected by decreased anti-NTHi Ig's within the lung. In addition, VDD led to an increase in total lung capacity (TLC), lung compliance (Cchord), MMP12/TIMP1 ratio with a rise in serum Ig titers and anti-dsDNA Ig's. Interestingly, in non-infected animals, VDD exacerbated the CS-induced anti-NTHi Ig's, anti-dsDNA Ig's and inflammatory cells within the lung. In COPD patients, serum Ig production was not affected by vitamin D status but anti-NTHi IgG increased after vitamin D3 supplementation in patients who were Vitamin D insufficient before treatment. During repeated infections, VDD facilitated NTHi eradication and resolution of local lung inflammation through production of anti-NTHi Ig, independently of CS whilst it also promoted autoantibodies.

Published
2022

39. High Serum Vitamin D Concentrations, Induced via Diet, Trigger Immune and Intestinal Microbiota Alterations Leading to Type 1 Diabetes Protection in NOD Mice

Author

Martens, Pieter-Jan, primary, Centelles-Lodeiro, Javier, additional, Ellis, Darcy, additional, Cook, Dana Paulina, additional, Sassi, Gabriele, additional, Verlinden, Lieve, additional, Verstuyf, Annemieke, additional, Raes, Jeroen, additional, Mathieu, Chantal, additional, and Gysemans, Conny, additional

Published
2022
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40. Additional file 10 of Effects of repeated infections with non-typeable Haemophilus influenzae on lung in vitamin D deficient and smoking mice

Author

Serr��, Jef, Tanjeko, Ajime Tom, Mathyssen, Carolien, Heigl, Tobias, Sacreas, Annelore, Cook, Dana Paulina, Verbeken, Erik, Maes, Karen, Verhaegen, Jan, Pilette, Charles, Vanoirbeek, Jeroen, Gysemans, Conny, Mathieu, Chantal, Vanaudenaerde, Bart, Janssens, Wim, and Gayan-Ramirez, Ghislaine

Abstract

Additional file 10: Table S1. Primer sequences (Series 2). Table S2. Baseline characteristics of the COPD patients in the placebo and vitamin D supplemented group. Table S3. Pro-inflammatory mediators in lung homogenate and serum of mice either vitamin D sufficient or deficient, repeatedly infected with NTHi and exposed either to CS or room air for 14 weeks (series 2)

Published
2022
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42. PTPN2 Regulates the Interferon Signaling and Endoplasmic Reticulum Stress Response in Pancreatic β-Cells in Autoimmune Diabetes

Author

Elvira, Bernat, primary, Vandenbempt, Valerie, primary, Bauzá-Martinez, Julia, primary, Crutzen, Raphaël, primary, Negueruela, Javier, primary, Ibrahim, Hazem, primary, Winder, Matthew L., primary, Brahma, Manoja K., primary, Vekeriotaite, Beata, primary, Martens, Pieter-Jan, primary, Singh, Sumeet Pal, primary, Rossello, Fernando, primary, Lybaert, Pascale, primary, Otonkoski, Timo, primary, Gysemans, Conny, primary, Wu, Wei, primary, and Gurzov, Esteban N., primary

Published
2022
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45. Macrophages are metabolically heterogeneous within the tumor microenvironment

Author

Geeraerts, Xenia, primary, Fernández-Garcia, Juan, additional, Hartmann, Felix J., additional, de Goede, Kyra E., additional, Martens, Liesbet, additional, Elkrim, Yvon, additional, Debraekeleer, Ayla, additional, Stijlemans, Benoit, additional, Vandekeere, Anke, additional, Rinaldi, Gianmarco, additional, De Rycke, Riet, additional, Planque, Mélanie, additional, Broekaert, Dorien, additional, Meinster, Elisa, additional, Clappaert, Emile, additional, Bardet, Pauline, additional, Murgaski, Aleksandar, additional, Gysemans, Conny, additional, Nana, Frank Aboubakar, additional, Saeys, Yvan, additional, Bendall, Sean C., additional, Laoui, Damya, additional, Van den Bossche, Jan, additional, Fendt, Sarah-Maria, additional, and Van Ginderachter, Jo A., additional

Published
2021
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46. Protocol to analyze circulating small non-coding RNAs by high-throughput RNA sequencing from human plasma samples

Author

Grieco, Giuseppina E., primary, Sebastiani, Guido, additional, Fignani, Daniela, additional, Brusco, Noemi, additional, Nigi, Laura, additional, Formichi, Caterina, additional, Licata, Giada, additional, Bruttini, Marco, additional, D’Aurizio, Romina, additional, Mathieu, Chantal, additional, Gysemans, Conny, additional, and Dotta, Francesco, additional

Published
2021
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47. Pro-inflammatory cytokines induce insulin and glucagon double positive human islet cells that are resistant to apoptosis

Author

Tesi, Marta, Bugliani, Marco, Ferri, Gianmarco, Suleiman, Mara, De Luca, Carmela, Bosi, Emanuele, Masini, Matilde, De Tata, Vincenzo, Gysemans, Conny, Cardarelli, Francesco, Cnop, Miriam, Eizirik, Decio L., Marchetti, Piero, Marselli, Lorella, Tesi, Marta, Bugliani, Marco, Ferri, Gianmarco, Suleiman, Mara, De Luca, Carmela, Bosi, Emanuele, Masini, Matilde, De Tata, Vincenzo, Gysemans, Conny, Cardarelli, Francesco, Cnop, Miriam, Eizirik, Decio L., Marchetti, Piero, and Marselli, Lorella

Abstract

The presence of islet cells double positive for insulin and glucagon (Ins+/Glu+) has been described in the pancreas from both type 2 (T2D) and type 1 (T1D) diabetic subjects. We studied the role of pro-inflammatory cytokines on the occurrence, trajectory, and characteristics of Ins+/Glu+ cells in human pancreatic islets. Pancreas samples, isolated islets, and dispersed islet cells from 3 T1D and 11 non-diabetic (ND) multi-organ donors were studied by immunofluorescence, confocal microscopy, and/or electron microscopy. ND islet cells were exposed to interleukin-1β and inter-feron-γ for up to 120 h. In T1D islets, we confirmed an increased prevalence of Ins+/Glu+ cells. Cyto-kine-exposed islets showed a progressive increase of Ins+/Glu+ cells that represented around 50% of endocrine cells after 120h. Concomitantly, cells expressing insulin granules only decreased significantly over time, whereas those containing only glucagon granules remained stable. Interestingly, Ins+/Glu+ cells were less prone to cytokine-induced apoptosis than cells containing only insulin. Cy-tokine-exposed islets showed down-regulation of β-cell identity genes. In conclusion, pro-inflam-matory cytokines induce Ins+/Glu+ cells in human islets, possibly due to a switch from a β-to a β-/α-cell phenotype. These Ins+/Glu+ cells appear to be resistant to cytokine-induced apoptosis., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2021

48. Macrophages are metabolically heterogeneous within the tumor microenvironment.

Author

UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Service de pneumologie, Geeraerts, Xenia, Fernández-Garcia, Juan, Hartmann, Felix J, de Goede, Kyra E, Martens, Liesbet, Elkrim, Yvon, Debraekeleer, Ayla, Stijlemans, Benoit, Vandekeere, Anke, Rinaldi, Gianmarco, De Rycke, Riet, Planque, Mélanie, Broekaert, Dorien, Meinster, Elisa, Clappaert, Emile, Bardet, Pauline, Murgaski, Aleksandar, Gysemans, Conny, Aboubakar Nana, Frank, Saeys, Yvan, Bendall, Sean C, Laoui, Damya, Van den Bossche, Jan, Fendt, Sarah-Maria, Van Ginderachter, Jo A, UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Service de pneumologie, Geeraerts, Xenia, Fernández-Garcia, Juan, Hartmann, Felix J, de Goede, Kyra E, Martens, Liesbet, Elkrim, Yvon, Debraekeleer, Ayla, Stijlemans, Benoit, Vandekeere, Anke, Rinaldi, Gianmarco, De Rycke, Riet, Planque, Mélanie, Broekaert, Dorien, Meinster, Elisa, Clappaert, Emile, Bardet, Pauline, Murgaski, Aleksandar, Gysemans, Conny, Aboubakar Nana, Frank, Saeys, Yvan, Bendall, Sean C, Laoui, Damya, Van den Bossche, Jan, Fendt, Sarah-Maria, and Van Ginderachter, Jo A

Abstract

Macrophages are often prominently present in the tumor microenvironment, where distinct macrophage populations can differentially affect tumor progression. Although metabolism influences macrophage function, studies on the metabolic characteristics of ex vivo tumor-associated macrophage (TAM) subsets are rather limited. Using transcriptomic and metabolic analyses, we now reveal that pro-inflammatory major histocompatibility complex (MHC)-II TAMs display a hampered tricarboxylic acid (TCA) cycle, while reparative MHC-II TAMs show higher oxidative and glycolytic metabolism. Although both TAM subsets rapidly exchange lactate in high-lactate conditions, only MHC-II TAMs use lactate as an additional carbon source. Accordingly, lactate supports the oxidative metabolism in MHC-II TAMs, while it decreases the metabolic activity of MHC-II TAMs. Lactate subtly affects the transcriptome of MHC-II TAMs, increases L-arginine metabolism, and enhances the T cell suppressive capacity of these TAMs. Overall, our data uncover the metabolic intricacies of distinct TAM subsets and identify lactate as a carbon source and metabolic and functional regulator of TAMs.

Published
2021

49. PTPN2 regulates the interferon signalling in pancreatic beta-cells and its expression correlates with therapy outcome in autoimmune diabetes

Author

Vandenbempt, Valerie, Elvira Jimenez, Bernat, Bauzá-Martinez, J., Negueruela Escudero, Javier, Ibrahim, Hazem, Winder, Matthew ML, Vekeriotaite, Beata, Singh, Sumeet Pal, Rossello, Fernando, Lybaert, Pascale, Otonkoski, Timo, Gysemans, Conny, Wu, Wei, Gurzov, Esteban Nicolas, Vandenbempt, Valerie, Elvira Jimenez, Bernat, Bauzá-Martinez, J., Negueruela Escudero, Javier, Ibrahim, Hazem, Winder, Matthew ML, Vekeriotaite, Beata, Singh, Sumeet Pal, Rossello, Fernando, Lybaert, Pascale, Otonkoski, Timo, Gysemans, Conny, Wu, Wei, and Gurzov, Esteban Nicolas

Abstract

info:eu-repo/semantics/published

Published
2021

50. Reversal of autoimmune diabetes by restoration of antigen-specific tolerance using genetically modified Lactococcus lactis in mice

Author

Takiishi, Tatiana, Korf, Hannelie, Belle, Tom Van L., Robert, Sofie, Grieco, Fabio A., Caluwaerts, Silvia, Galleri, Letizia, Spagnuolo, Isabella, Steidler, Lothar, Huynegem, Karolien Van, Demetter, Pieter, Wasserfall, Clive, Atkinson, Mark A., Dotta, Francesco, Rottiers, Pieter, Gysemans, Conny, and Mathieu, Chantal

Subjects
Drugs -- Vehicles, Type 1 diabetes -- Care and treatment -- Research, Antigens -- Dosage and administration -- Research, Lactococcus -- Usage -- Research, Drug delivery systems -- Research, Genetically modified organisms -- Usage -- Research, Health care industry
Abstract

Current interventions for arresting autoimmune diabetes have yet to strike the balance between sufficient efficacy, minimal side effects, and lack of generalized immunosuppression. Introduction of antigen via the gut represents an appealing method for induction of antigen-specific tolerance. Here, we developed a strategy for tolerance restoration using mucosal delivery in mice of biologically contained Lactococcus lactis genetically modified to secrete the whole proinsulin autoantigen along with the immunomodulatory cytokine IL-10. We show that combination therapy with low-dose systemic anti-CD3 stably reverted diabetes in NOD mice and increased frequencies of local Tregs, which not only accumulated in the pancreatic islets, but also suppressed immune response in an autoantigen-specific way. Cured mice remained responsive to disease-unrelated antigens, which argues against excessive immunosuppression. Application of this therapeutic tool achieved gut mucosal delivery of a diabetes-relevant autoantigen and a biologically active immunomodulatory cytokine, IL-10, and, when combined with a low dose of systemic anti-CD3, was well tolerated and induced autoantigen-specific long-term tolerance, allowing reversal of established autoimmune diabetes. Therefore, we believe this method could be an effective treatment strategy for type 1 diabetes in humans., Introduction Type 1 diabetes (T1D) is an autoimmune disease characterized by breach in tolerance toward pancreatic insulin-producing [beta] cells (1, 2). Interventions aimed at arresting [beta] cell destruction once the [...]

Published
2012
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