0000000000871131

AUTHOR

Oliver Schanz

showing 2 related works from this author

Liver-primed memory T cells generated under noninflammatory conditions provide anti-infectious immunity.

2013

SummaryDevelopment of CD8+ T cell (CTL) immunity or tolerance is linked to the conditions during T cell priming. Dendritic cells (DCs) matured during inflammation generate effector/memory T cells, whereas immature DCs cause T cell deletion/anergy. We identify a third outcome of T cell priming in absence of inflammation enabled by cross-presenting liver sinusoidal endothelial cells. Such priming generated memory T cells that were spared from deletion by immature DCs. Similar to central memory T cells, liver-primed T cells differentiated into effector CTLs upon antigen re-encounter on matured DCs even after prolonged absence of antigen. Their reactivation required combinatorial signaling thro…

T cellReceptors Antigen T-CellPriming (immunology)chemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationGeneral Biochemistry Genetics and Molecular BiologyMiceCross-PrimingAntigenCD28 AntigensmedicineAnimalslcsh:QH301-705.5Innate immune systemGene Expression ProfilingT-cell receptorReceptors Interleukin-12CD28Endothelial Cellshemic and immune systemsDendritic CellsAcquired immune systemListeria monocytogenesImmunity InnateNeuropilin-1Mice Inbred C57BLmedicine.anatomical_structurelcsh:Biology (General)LiverImmunologyImmunologic MemoryCD8Cell reports
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Enzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.

2019

Summary Regulatory T cells (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific suppressive mechanisms is unclear. Here, we found that the enzyme hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes prostaglandin E2 (PGE2) into the metabolite 15-keto PGE2, was highly expressed in Treg cells, particularly those in visceral adipose tissue (VAT). Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE2 suppressed conventional T cell activation and proliferation. C…

0301 basic medicineanalogs & derivatives [Dinoprostone]Malemetabolism [Diabetes Mellitus Type 2]Adipose tissueLymphocyte Activation15-ketoprostaglandin E2T-Lymphocytes RegulatoryJurkat cellsJurkat CellsMice0302 clinical medicineimmunology [Lymphocyte Activation]genetics [Insulin Resistance]STAT5 Transcription FactorHomeostasisImmunology and AllergyTissue homeostasisgenetics [Hydroxyprostaglandin Dehydrogenases]Mice Knockoutcytology [Intra-Abdominal Fat]enzymology [T-Lymphocytes Regulatory]FOXP3hemic and immune systems3T3 CellsCell biologyInfectious Diseases030220 oncology & carcinogenesisHydroxyprostaglandin Dehydrogenasesmedicine.symptomimmunology [T-Lymphocytes Regulatory]metabolism [STAT5 Transcription Factor]Immunologymetabolism [Dinoprostone]chemical and pharmacologic phenomenaInflammationIntra-Abdominal FatBiologyDinoprostoneCell Line03 medical and health sciencesmetabolism [Hydroxyprostaglandin Dehydrogenases]immunology [Homeostasis]medicineAnimalsHumansddc:610immunology [Intra-Abdominal Fat]HEK 293 cells030104 developmental biologyHEK293 CellsDiabetes Mellitus Type 2Cell cultureInsulin ResistanceHomeostasis
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