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Reactive oxygen species-dependent Toll/NF-κB activation in the Drosophila hematopoietic niche confers resistance to wasp parasitism

Hematopoietic stem/progenitor cells in the adult mammalian bone marrow ensure blood cell renewal. Their cellular microenvironment, called 'niche', regulates hematopoiesis both under homeostatic and immune stress conditions. In the hematopoietic organ, the lymph gland, the posterior signali...

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Published in:	eLife 2017-11, Vol.6
Main Authors:	Louradour, Isabelle, Sharma, Anurag, Morin-Poulard, Ismael, Letourneau, Manon, Vincent, Alain, Crozatier, Michèle, Vanzo, Nathalie
Format:	Article
Language:	English
Subjects:	Animals Blood Bone marrow Drosophila Drosophila - immunology Drosophila - parasitology Drosophila Proteins - metabolism Eggs Epidermal growth factor receptors ErbB Receptors - metabolism Experiments Hematopoiesis Hematopoietic stem cells Host-Parasite Interactions Immune response Immunity, Innate Insects Leptopilina boulardi Ligands Lymph Lymph gland NF-kappa B - metabolism NF-κB protein Parasitism Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Invertebrate Peptide - metabolism Stem Cells and Regenerative Medicine Toll-Like Receptors - metabolism Toll/NF-kB pathway Wasps - immunology
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description	Hematopoietic stem/progenitor cells in the adult mammalian bone marrow ensure blood cell renewal. Their cellular microenvironment, called 'niche', regulates hematopoiesis both under homeostatic and immune stress conditions. In the hematopoietic organ, the lymph gland, the posterior signaling center (PSC) acts as a niche to regulate the hematopoietic response to immune stress such as wasp parasitism. This response relies on the differentiation of lamellocytes, a cryptic cell type, dedicated to pathogen encapsulation and killing. Here, we establish that Toll/NF-κB pathway activation in the PSC in response to wasp parasitism non-cell autonomously induces the lymph gland immune response. Our data further establish a regulatory network where co-activation of Toll/NF-κB and EGFR signaling by ROS levels in the PSC/niche controls lymph gland hematopoiesis under parasitism. Whether a similar regulatory network operates in mammals to control emergency hematopoiesis is an open question.
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Their cellular microenvironment, called 'niche', regulates hematopoiesis both under homeostatic and immune stress conditions. In the hematopoietic organ, the lymph gland, the posterior signaling center (PSC) acts as a niche to regulate the hematopoietic response to immune stress such as wasp parasitism. This response relies on the differentiation of lamellocytes, a cryptic cell type, dedicated to pathogen encapsulation and killing. Here, we establish that Toll/NF-κB pathway activation in the PSC in response to wasp parasitism non-cell autonomously induces the lymph gland immune response. Our data further establish a regulatory network where co-activation of Toll/NF-κB and EGFR signaling by ROS levels in the PSC/niche controls lymph gland hematopoiesis under parasitism. 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subjects	Animals Blood Bone marrow Drosophila Drosophila - immunology Drosophila - parasitology Drosophila Proteins - metabolism Eggs Epidermal growth factor receptors ErbB Receptors - metabolism Experiments Hematopoiesis Hematopoietic stem cells Host-Parasite Interactions Immune response Immunity, Innate Insects Leptopilina boulardi Ligands Lymph Lymph gland NF-kappa B - metabolism NF-κB protein Parasitism Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Invertebrate Peptide - metabolism Stem Cells and Regenerative Medicine Toll-Like Receptors - metabolism Toll/NF-kB pathway Wasps - immunology
title	Reactive oxygen species-dependent Toll/NF-κB activation in the Drosophila hematopoietic niche confers resistance to wasp parasitism
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