F
Frederic Geissmann
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 153
Citations - 43031
Frederic Geissmann is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Monocyte & Macrophage. The author has an hindex of 73, co-authored 147 publications receiving 37781 citations. Previous affiliations of Frederic Geissmann include New York University & University of Paris.
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Journal ArticleDOI
Tissue-resident macrophages originate from yolk-sac-derived erythro-myeloid progenitors
Elisa Gomez Perdiguero,Kay Klapproth,Christian Schulz,Katrin Busch,Emanuele Azzoni,Lucile Crozet,Hannah Garner,Céline Trouillet,Marella F. T. R. de Bruijn,Frederic Geissmann,Hans Reimer Rodewald +10 more
TL;DR: It is shown in mice that the vast majority of adult tissue-resident macrophages originate from a Tie2+ (also known as Tek) cellular pathway generating Csf1r+ erythro-myeloid progenitors (EMPs) distinct from HSCs.
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Blood monocytes: development, heterogeneity, and relationship with dendritic cells.
TL;DR: Functional characterization of monocytes is in progress in humans and rodents and will provide a better understanding of the pathophysiology of inflammation.
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Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).
Patrick Revy,Taro Muto,Yves Levy,Frederic Geissmann,Alessandro Plebani,Ozden Sanal,Nadia Catalan,Monique Forveille,Dufourcq-Lagelouse R,Andrew R. Gennery,Ilhan Tezcan,Fügen Ersoy,Hülya Kayserili,Alberto G. Ugazio,Nicole Brousse,Masamichi Muramatsu,Luigi D. Notarangelo,Kazuo Kinoshita,Tasuku Honjo,Alain Fischer,Anne Durandy +20 more
TL;DR: The phenotype observed in HIGM2 patients (and in AID-/- mice) demonstrates the absolute requirement for AID in several crucial steps of B cell terminal differentiation necessary for efficient antibody responses.
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Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors.
Jérôme Cros,Nicolas Cagnard,Kevin J. Woollard,Natacha Patey,Shen-Ying Zhang,Brigitte Senechal,Anne Puel,Subhra K. Biswas,Despina Moshous,Capucine Picard,Jean-Philippe Jais,David D'Cruz,Jean-Laurent Casanova,Jean-Laurent Casanova,Jean-Laurent Casanova,Céline Trouillet,Frederic Geissmann,Frederic Geissmann +17 more
TL;DR: CD14dim monocytes were weak phagocytes and did not produce ROS or cytokines in response to cell-surface Toll-like receptors, but selectively produced TNF-α, IL-1β, and CCL3 inresponse to viruses and immune complexes containing nucleic acids, via a proinflammatory TLR7-TLR 8-MyD88-MEK pathway.
Journal ArticleDOI
Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathways
Katrin Kierdorf,Daniel Erny,Tobias Goldmann,Victor Sander,Christian Schulz,Elisa Gomez Perdiguero,Peter Wieghofer,Annette Heinrich,Pia Riemke,Christoph Hölscher,Dominik N. Müller,Bruno Luckow,Thomas Brocker,Katharina Debowski,Günter Fritz,Ghislain Opdenakker,Andreas Diefenbach,Knut Biber,Knut Biber,Mathias Heikenwalder,Frederic Geissmann,Frank Rosenbauer,Marco Prinz +22 more
TL;DR: It is found that mouse microglia were derived from primitive c-kit+ erythromyeloid precursors that were detected in the yolk sac as early as 8 d post conception and microgliogenesis was not only dependent on the transcription factor Pu.1, but also required Irf8, which was vital for the development of the A2 population, whereas Myb, Id2, Batf3 and Klf4 were not required.