0000000000017372

AUTHOR

Emmanuel Pinteaux

0000-0002-9986-4401

showing 3 related works from this author

Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses

2017

Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, b…

0301 basic medicineLipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharideFeverCell- och molekylärbiologiImmunologyHypothalamusAnorexiaEtanerceptInterleukin-1 type 1 receptor; Lipopolysaccharide; Fever; Anorexia; ACTH; Corticosterone; Endothelial cells; THF alpha; Interleukin-6; PGE(2)03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundEating0302 clinical medicineAdrenocorticotropic HormoneCorticosteroneInternal medicinemedicineJournal ArticleAnimalsInterleukin 6ReceptorIllness BehaviorInflammationMice KnockoutReceptors Interleukin-1 Type IbiologyEndocrine and Autonomic Systemsbusiness.industryInterleukinBrainEndothelial CellsAnorexia030104 developmental biologyEndocrinologychemistrybiology.proteinTumor necrosis factor alphaFemalemedicine.symptomInflammation MediatorsbusinessCorticosterone030217 neurology & neurosurgeryCell and Molecular Biologymedicine.drug
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IL ‐1 signaling is critical for expansion but not generation of autoreactive GM ‐ CSF + Th17 cells

2016

Abstract Interleukin‐1 (IL‐1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL‐1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL‐1 receptor type 1 (IL‐1R1)‐dependent IL‐1β expression by myeloid cells in the draining lymph nodes. This myeloid‐derived IL‐1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM‐CSF + Th17 cell subset, thereby enhancing its encephalitog…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalBiologymedicine.disease_causePertussis toxinGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityMice03 medical and health sciences0302 clinical medicineMediatormedicineAnimalsInducerMolecular BiologyCell ProliferationGeneral Immunology and MicrobiologyGeneral NeuroscienceMultiple sclerosisExperimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorArticlesmedicine.diseaseCell biology030104 developmental biologyPertussis ToxinT cell subsetImmunologyTh17 CellsLymphInterleukin-1030215 immunologyThe EMBO Journal
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Genetic Cell Ablation Reveals Clusters of Local Self-Renewing Microglia in the Mammalian Central Nervous System

2015

SummaryDuring early embryogenesis, microglia arise from yolk sac progenitors that populate the developing central nervous system (CNS), but how the tissue-resident macrophages are maintained throughout the organism’s lifespan still remains unclear. Here, we describe a system that allows specific, conditional ablation of microglia in adult mice. We found that the microglial compartment was reconstituted within 1 week of depletion. Microglia repopulation relied on CNS-resident cells, independent from bone-marrow-derived precursors. During repopulation, microglia formed clusters of highly proliferative cells that migrated apart once steady state was achieved. Proliferating microglia expressed …

Central Nervous SystemCellular differentiationCentral nervous systemInterleukin-1betaImmunologyCX3C Chemokine Receptor 1Bone Marrow CellsBiologyMiceCell MovementCX3CR1medicineAnimalsImmunology and AllergyProgenitor cellNeuroinflammationCell ProliferationReceptors Interleukin-1 Type IMicrogliaBase SequenceTumor Necrosis Factor-alphaMacrophagesCell DifferentiationSequence Analysis DNAHematopoietic Stem CellsCell biologyMice Inbred C57BLmedicine.anatomical_structureInfectious DiseasesImmunologyTumor necrosis factor alphaReceptors ChemokineMicrogliaSignal transductionSignal TransductionImmunity
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