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Your search keyword '"Benabid, Adam"' showing total 14 results
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14 results on '"Benabid, Adam"'

2. Non-canonical Hedgehog signaling mediates profibrotic hematopoiesis-stroma crosstalk in myeloproliferative neoplasms

Author

Pritchard, Jessica E., Pearce, Juliette E., Snoeren, Inge A.M., Fuchs, Stijn N.R., Götz, Katrin, Peisker, Fabian, Wagner, Silke, Benabid, Adam, Lutterbach, Niklas, Klöker, Vanessa, Nagai, James S., Hannani, Monica T., Galyga, Anna K., Sistemich, Ellen, Banjanin, Bella, Flosdorf, Niclas, Bindels, Eric, Olschok, Kathrin, Biaesch, Katharina, Chatain, Nicolas, Bhagwat, Neha, Dunbar, Andrew, Sarkis, Rita, Naveiras, Olaia, Berres, Marie-Luise, Koschmieder, Steffen, Levine, Ross L., Costa, Ivan G., Gleitz, Hélène F.E., Kramann, Rafael, and Schneider, Rebekka K.

Published
2024
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3. M cell maturation and cDC activation determine the onset of adaptive immune priming in the neonatal Peyer’s patch

Author

Torow, Natalia, Li, Ronghui, Hitch, Thomas Charles Adrian, Mingels, Clemens, Al Bounny, Shahed, van Best, Niels, Stange, Eva-Lena, Simons, Britta, Maié, Tiago, Rüttger, Lennart, Gubbi, Narasimha Murthy Keshava Prasad, Abbott, Darryl Adelaide, Benabid, Adam, Gadermayr, Michael, Runge, Solveig, Treichel, Nicole, Merhof, Dorit, Rosshart, Stephan Patrick, Jehmlich, Nico, Hand, Timothy Wesley, von Bergen, Martin, Heymann, Felix, Pabst, Oliver, Clavel, Thomas, Tacke, Frank, Lelouard, Hugues, Costa, Ivan Gesteira, and Hornef, Mathias Walter

Published
2023
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5. Non-Canonical Hedgehog Signaling Mediates Profibrotic Hematopoiesis-Stroma Crosstalk in Myeloproliferative Neoplasms

Author

Pritchard, Jessica E., primary, Pearce, Juliette E., additional, Snoeren, Inge A.M., additional, Fuchs, Stijn N.R., additional, Götz, Katrin, additional, Peisker, Fabian, additional, Wagner, Silke, additional, Benabid, Adam, additional, Lutterbach, Niklas, additional, Galyga, Anna K., additional, Nagai, James S., additional, Krämer, Vanessa, additional, Hannani, Monica T., additional, Bindels, Eric, additional, Olschok, Kathrin, additional, Chatain, Nicolas, additional, Bhagwat, Neha, additional, Dunbar, Andrew, additional, Berres, Marie-Luise, additional, Koschmieder, Steffen, additional, Levine, Ross L., additional, Costa, Ivan, additional, Gleitz, Hélène F.E., additional, Kramann, Rafael, additional, and Schneider, Rebekka, additional

Published
2023
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6. PDGFRα-induced stromal maturation is required to restrain postnatal intestinal epithelial stemness and promote defense mechanisms

Author

Jacob, Jean-Marie, primary, Di Carlo, Selene E., additional, Stzepourginski, Igor, additional, Lepelletier, Anthony, additional, Ndiaye, Papa Diogop, additional, Varet, Hugo, additional, Legendre, Rachel, additional, Kornobis, Etienne, additional, Benabid, Adam, additional, Nigro, Giulia, additional, and Peduto, Lucie, additional

Published
2022
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7. Neonatal Peyer's patch cDC activation as a pacemaker of postnatal immune maturation

Author

Torow, Natalia, Li, Ronghui, Hitch, Thomas, Mingels, Clemens, Al Bounny, Shahed, van Best, Niels, Stange, Eva-Lena, Benabid, Adam, Ruettger, Lennart, Gadermayr, Michael, Runge, S., Treichel, N., Merhof, D., Rosshart, S., Jehmlich, N., von Bergen, M., Heymann, F., Clavel, T., Tacke, F., Lelouard, H., Costa, Ivan G., and Hornef, M. W.

Abstract

Cold Spring Harbor : Cold Spring Harbor Laboratory, bioRxiv : the preprint server for biology 1-41 (2022). doi:10.1101/2022.03.03.482839, Published by Cold Spring Harbor Laboratory, Cold Spring Harbor

Published
2022
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8. Inflammation drives pressure on TP53mutant clones in myeloproliferative neoplasms

Author

Benabid, Adam and Schneider, Rebekka K.

Abstract

Transformation of a myeloproliferative neoplasm to a secondary acute myeloid leukemia is rare but devastating. Single-cell, multi-omic characterization of hematopoietic stem and progenitor cells now shows the role of inflammation in transformation driven by mutations in TP53, with effects on the mutant clone but also non-mutant counterparts.

Published
2023
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10. Still a burning question:the interplay between inflammation and fibrosis in myeloproliferative neoplasms

Author

Gleitz, Hélène F.E., Benabid, Adam, Schneider, Rebekka K., Gleitz, Hélène F.E., Benabid, Adam, and Schneider, Rebekka K.

Abstract

PURPOSE OF REVIEW: Bone marrow fibrosis is the progressive replacement of blood-forming cells by reticulin fibres, caused by the acquisition of somatic mutations in hematopoietic stem cells. The molecular and cellular mechanisms that drive the progression of bone marrow fibrosis remain unknown, yet chronic inflammation appears to be a conserved feature in most patients suffering from myeloproliferative neoplasms. RECENT FINDINGS: Here, we review recent literature pertaining to the role of inflammation in driving bone marrow fibrosis, and its effect on the various hematopoietic and nonhematopoietic cell populations. SUMMARY: Recent evidence suggests that the pathogenesis of MPN is primarily driven by the hematopoietic stem and progenitor cells, together with their mutated progeny, which in turn results in chronic inflammation that disrupts the bone marrow niche and perpetuates a disease-permissive environment. Emerging data suggests that specifically targeting stromal inflammation in combination with JAK inhibition may be the way forward to better treat MPNs, and bone marrow fibrosis specifically.

Published
2021

12. cAMP bursts control T cell directionality by actin cytoskeleton remodeling

Author

Simao, Morgane, primary, Régnier, Fabienne, additional, Taheraly, Sarah, additional, Fraisse, Achille, additional, Tacine, Rachida, additional, Fraudeau, Marie, additional, Benabid, Adam, additional, Feuillet, Vincent, additional, Lambert, Mireille, additional, Delon, Jérôme, additional, and Randriamampita, Clotilde, additional

Published
2020
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14. Non-Canonical Hedgehog Signaling Mediates Profibrotic Hematopoiesis-Stroma Crosstalk in Myeloproliferative Neoplasms

Author

Pritchard, Jessica E., Pearce, Juliette E., Snoeren, Inge A.M., Fuchs, Stijn N.R., Götz, Katrin, Peisker, Fabian, Wagner, Silke, Benabid, Adam, Lutterbach, Niklas, Klöker, Vanessa, Nagai, James S., Hannani, Monica T., Galyga, Anna K., Sistemich, Ellen, Banjanin, Bella, Flosdorf, Niclas, Bindels, Eric, Olschok, Kathrin, Biaesch, Katharina, Chatain, Nicolas, Bhagwat, Neha, Dunbar, Andrew, Sarkis, Rita, Naveiras, Olaia, Berres, Marie-Luise, Koschmieder, Steffen, Levine, Ross L., Costa, Ivan G., Gleitz, Hélène F.E., Kramann, Rafael, and Schneider, Rebekka K.

Abstract

The role of hematopoietic hedgehog signaling in MPN remains incompletely understood despite data suggesting Hh pathway inhibitors have therapeutic activity in patients. We aim to systematically interrogate the role of canonical vs. non canonical Hh signaling in MPN. We show that Gli1 protein levels in patient PBMCs mark fibrotic progression and that in murine MPN models, absence of hematopoietic Gli1, but not Gli2or Smo, significantly reduces MPN phenotype and fibrosis, indicating that GLI1 in the MPN clone can be activated in a non-canonical fashion. Additionally, we establish that hematopoietic Gli1has a significant effect on stromal cells, mediated through a druggable MIF/CD74 axis. These data highlight the complex interplay between alterations in the MPN clone and activation of stromal cells and indicate Gli1represents a promising therapeutic target in MPN, particularly Hh signaling is dispensable for normal hematopoiesis.

Published
2023
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