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Type I IFN signaling triggers immunopathology in tuberculosis-susceptible mice by modulating lung phagocyte dynamics

MPS-Authors
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Dorhoi,  Anca
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Yeremeev,  Vladimir
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Nouailles,  Geraldine
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Weiner,  January 3rd
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Jörg,  Sabine
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Heinemann,  Ellen
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Oberbeck-Müller,  Dagmar
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Knaul,  Julia K.
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Vogelzang,  Alexis
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Reece,  Stephen T.
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Hahnke,  Karin
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Mollenkopf,  Hans-Joachim
Core Facilities / Microarray, Max Planck Institute for Infection Biology, Max Planck Society;

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Brinkmann,  Volker
Core Facilities / Microscopy, Max Planck Institute for Infection Biology, Max Planck Society;

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Kaufmann,  Stefan H. E.
Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Citation

Dorhoi, A., Yeremeev, V., Nouailles, G., Weiner, J. 3., Jörg, S., Heinemann, E., et al. (2014). Type I IFN signaling triggers immunopathology in tuberculosis-susceptible mice by modulating lung phagocyte dynamics. European Journal of Immunology, 44(8), 2380-2393. doi:10.1002/eji.201344219.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0023-E05C-0
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