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AUTHOR

Leif Rogell

showing 3 related works from this author

Differentiation of Type 1 ILCs from a Common Progenitor to All Helper-like Innate Lymphoid Cell Lineages

2014

SummaryInnate lymphoid cells (ILCs) are a recently recognized group of lymphocytes that have important functions in protecting epithelial barriers against infections and in maintaining organ homeostasis. ILCs have been categorized into three distinct groups, transcriptional circuitry and effector functions of which strikingly resemble the various T helper cell subsets. Here, we identify a common, Id2-expressing progenitor to all interleukin 7 receptor-expressing, “helper-like” ILC lineages, the CHILP. Interestingly, the CHILP differentiated into ILC2 and ILC3 lineages, but not into conventional natural killer (cNK) cells that have been considered an ILC1 subset. Instead, the CHILP gave rise…

Cellular differentiationLineage (evolution)Bone Marrow CellsGATA3 Transcription FactorBiologyGeneral Biochemistry Genetics and Molecular BiologyMicemedicineAnimalsLymphocytesskin and connective tissue diseasesProgenitorInhibitor of Differentiation Protein 2Receptors Interleukin-7Biochemistry Genetics and Molecular Biology(all)Intracellular parasiteStem CellsInnate lymphoid cellNFIL3Cell DifferentiationT helper cellImmunity InnateMice Inbred C57BLbody regionsmedicine.anatomical_structureImmunologyToxoplasmaIntracellularToxoplasmosisCell
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Microbiota-Induced Type I Interferons Instruct a Poised Basal State of Dendritic Cells

2019

Summary Environmental signals shape host physiology and fitness. Microbiota-derived cues are required to program conventional dendritic cells (cDCs) during the steady state so that they can promptly respond and initiate adaptive immune responses when encountering pathogens. However, the molecular underpinnings of microbiota-guided instructive programs are not well understood. Here, we report that the indigenous microbiota controls constitutive production of type I interferons (IFN-I) by plasmacytoid DCs. Using genome-wide analysis of transcriptional and epigenetic regulomes of cDCs from germ-free and IFN-I receptor (IFNAR)-deficient mice, we found that tonic IFNAR signaling instructs a spec…

MaleReceptor Interferon alpha-betaAdaptive ImmunityCD8-Positive T-LymphocytesBiologyGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineImmune systemAntigenAnimalsEpigeneticsReceptor030304 developmental biologyEpigenomics0303 health sciencesMicrobiotaPeripheral toleranceDendritic Cellsperipheral toleranceCell biologyMice Inbred C57BLtype I interferonsplasmacytoid dendritic cellsconventional dendritic cellsInterferon Type IFemale030217 neurology & neurosurgerySignal TransductionCell
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DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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