0000000000676589

AUTHOR

Sabine Ring

showing 4 related works from this author

Regulatory T cell-derived adenosine induces dendritic cell migration through the Epac-Rap1 pathway.

2014

Abstract Dendritic cells (DC) are one target for immune suppression by regulatory T cells (Treg), because their interaction results in reduced T cell stimulatory capacity and secretion of inhibitory cytokines in DC. We show that DC in the presence of Treg are more mobile as compared with cocultures with conventional CD4+ T cells and form DC–Treg aggregates within 2 h of culture. The migration of DC was specifically directed toward Treg, as Treg, but not CD4+ T cells, attracted DC in Boyden chambers. Treg deficient for the ectonucleotidase CD39 were unable to attract DC. Likewise, addition of antagonists for A2A adenosine receptors abolished the formation of DC–Treg clusters, indicating a ro…

AdenosineRegulatory T cellT cellImmunologyMedizinchemical and pharmacologic phenomenaCell CommunicationBiologyT-Lymphocytes RegulatoryMiceAdenosine TriphosphateAntigens CDCell MovementmedicineImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsDendritic cell migrationReceptors Adenosine A2Apyraserap1 GTP-Binding Proteinshemic and immune systemsDendritic CellsActin cytoskeletonAdenosineAdenosine receptorCell biologyActin Cytoskeletonmedicine.anatomical_structureRap1Signal transductionmedicine.drugSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
researchProduct

Regulatory T Cells Prevent Neutrophilic Infiltration of Skin during Contact Hypersensitivity Reactions by Strengthening the Endothelial Barrier

2020

The healing phase of contact hypersensitivity reactions is critically dependent on regulatory T cells (Tregs), but even the early inflammatory phase, that is, 6-24 hours after induction of a contact hypersensitivity reaction, is susceptible to Treg-mediated suppression. To investigate the underlying mechanisms, we injected Tregs before the challenge and analyzed the skin-infiltrating cells as early as 6 hours later. Early on, we found mainly neutrophils in the challenged skin, but only a few T cells. This influx of neutrophils was blocked by the injection of Tregs, indicating that they were able to prevent the first wave of leukocytes, which are responsible for starting an immune reaction. …

0301 basic medicineNeutrophilsRegulatory T cellchemical and pharmacologic phenomenaCell CommunicationPicryl ChlorideDermatologyFilaminT-Lymphocytes RegulatoryBiochemistryProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationNectinmedicineAnimalsHumansProtein kinase AMolecular BiologySkinChemistryChemotaxisCell BiologyCell biologyEndothelial stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisDermatitis Allergic ContactEndothelium VascularIntracellularJournal of Investigative Dermatology
researchProduct

Down-Regulation of CD62L Shedding in T Cells by CD39+ Regulatory T Cells Leads to Defective Sensitization in Contact Hypersensitivity Reactions

2016

Injection of regulatory T cells (Tregs) followed by sensitization with 2,4,6-trinitrochlorobenzene induced a transient increase in size and cellularity of skin-draining lymph nodes (LNs) in mice. This led us to hypothesize that Tregs may affect the trafficking of T cells from and to peripheral LNs. Two to three hours after sensitization, we found fewer CD8+ T cells expressing CD62L in LNs compared with untreated controls. Injection of wild-type Tregs prevented this down-regulation of CD62L. In contrast, Tregs devoid of the adenosine triphosphate (ATP)-degrading ecto-enzyme CD39 were unable to do so. As for the mechanism of CD62L regulation, we found that ATP, which is released in skin upon …

0301 basic medicineRegulatory T cellBlotting WesternMedizinDown-Regulationchemical and pharmacologic phenomenaDermatologyT-Lymphocytes RegulatoryBiochemistryArticleMice03 medical and health scienceschemistry.chemical_compoundAdenosine Triphosphate0302 clinical medicineImmune systemDownregulation and upregulationAntigenAntigens CDReference ValuesmedicineAnimalsImmunologic FactorsL-SelectinMolecular BiologyCells CulturedSensitizationintegumentary systemChemistryApyrasehemic and immune systemsCell BiologyDendritic cellFlow CytometryCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEpidermal CellsDermatitis Allergic ContactImmunologyImmunizationLymph NodesEpidermisAdenosine triphosphateCD8030215 immunologyJournal of Investigative Dermatology
researchProduct

Production of Extracellular Adenosine by CD73+ Dendritic Cells Is Crucial for Induction of Tolerance in Contact Hypersensitivity Reactions

2019

Dendritic cells (DCs) express the ecto-5′-nucleotidase CD73 that generates immunosuppressive adenosine (Ado) by dephosphorylation of extracellular Ado monophosphate and diphosphate. To investigate whether CD73-derived Ado has immune-suppressive activity, 2,4-dinitrothiocyanobenzene (DNTB) was applied to skin of wild-type (WT) or CD73-deficient (CD73–/–) mice, followed by sensitization and challenge with 2,4-dinitrofluorobenzene. In this model, we show the induction of tolerance by DNTB against 2,4-dinitrofluorobenzene only in WT but not in CD73–/– mice. Analysis of skin DCs showed increased expression of CD73 after application of DNTB in WT mice. That was accompanied by elevated concentrati…

0301 basic medicineAdenosine monophosphateLangerhans cellRegulatory T cellTransgeneCell BiologyDermatologyDendritic cellBiochemistryAdenosineCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structurechemistry030220 oncology & carcinogenesisExtracellularmedicineCyclic adenosine monophosphateMolecular Biologymedicine.drugJournal of Investigative Dermatology
researchProduct