0000000000288570

AUTHOR

Nicola Hoppmann

showing 3 related works from this author

New candidates for CD4 T cell pathogenicity in experimental neuroinflammation and multiple sclerosis

2015

Multiple sclerosis is a chronic autoimmune demyelinating disease of the central nervous system, which is thought to be triggered by environmental factors in genetically susceptible individuals leading to activation of autoreactive T lymphocytes. Large multi-centre genome-wide association studies have identified multiple genetic risk loci in multiple sclerosis. In this study, we investigated T cell transcriptomic changes in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. We correlated these findings with the multiple sclerosis risk genes postulated by the most recent Immunochip analysis and found that multiple sclerosis susceptibility genes were significant…

CD4-Positive T-LymphocytesMice KnockoutEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEffectorMultiple sclerosisT cellExperimental autoimmune encephalomyelitisGenome-wide association studyMERTKBiologymedicine.diseaseMice Inbred C57BLMicemedicine.anatomical_structureImmunologymedicineDemyelinating diseaseAnimalsHumansGene Regulatory NetworksNeurology (clinical)NeuroinflammationBrain
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Gatekeeper role of brain antigen‐presenting CD11c + cells in neuroinflammation

2015

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesAntigen-Presenting CellsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInterleukin 210302 clinical medicineCell MovementAnimalsCytotoxic T cellAntigen-presenting cellMolecular BiologyNeuroinflammationInterleukin 3CD40General Immunology and MicrobiologybiologyGeneral NeuroscienceInterleukin-17BrainGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsDendritic CellsArticlesNatural killer T cellCD11c AntigenMice Inbred C57BL030104 developmental biologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 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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