0000000000408201

AUTHOR

Sabine Zahn

showing 8 related works from this author

Resistance to water and abrasion of a broad-spectrum sunscreen: a prospective, open-label study.

2015

1303 BiochemistryFrictionAbrasion (mechanical)Ultraviolet RaysDrug Evaluation PreclinicalSunburn610 Medicine & healthSunscreening AgentsDermatologyAdministration Cutaneous030226 pharmacology & pharmacyBiochemistry2708 Dermatology03 medical and health sciencesBroad spectrum0404 agricultural biotechnology0302 clinical medicineOpen label study1312 Molecular BiologymedicineHumansProspective StudiesSunburnComposite materialMolecular BiologySkin damageSkinWater resistanceChemistry10177 Dermatology ClinicWater04 agricultural and veterinary sciencesmedicine.disease040401 food scienceLiposomesHydrophobic and Hydrophilic InteractionsSunscreening AgentsExperimental dermatology
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Dendritic cell-derived IL-12p40 homodimer contributes to susceptibility in cutaneous leishmaniasis in BALB/c mice

2007

Abstract Protection against Leishmania major in resistant C57BL/6 mice is mediated by Th1 cells, whereas susceptibility in BALB/c mice is the result of Th2 development. IL-12 release by L. major-infected dendritic cells (DC) is critically involved in differentiation of Th1 cells. Previously, we reported that strain differences in the production of DC-derived factors, e.g., IL-1αβ, are in part responsible for disparate disease outcome. In the present study, we analyzed the release of IL-12 from DC in more detail. Stimulated DC from C57BL/6 and BALB/c mice released comparable amounts of IL-12p40 and p70. In the absence of IL-4, BALB/c DC produced significantly more IL-12p40 than C57BL/6 DC. D…

TransgeneImmunologyLeishmaniasis CutaneousMice TransgenicBiologyBALB/cMiceWestern blotSpecies SpecificityIn vivoImmunitymedicineImmunology and AllergyAnimalsLeishmania majorGenetic Predisposition to DiseaseCells CulturedLeishmania majorMice Inbred BALB Cmedicine.diagnostic_testInterleukin-12 Subunit p40Dendritic cellDendritic Cellsbiology.organism_classificationMolecular biologyInterleukin-12In vitroImmunity InnateMice Inbred C57BLImmunologyInterleukin-4DimerizationSignal Transduction
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Thiol antioxidants block the activation of antigen-presenting cells by contact sensitizers.

2003

Strong contact sensitizers are able to induce signal transduction mechanisms such as tyrosine phosphorylation and activation of MAP kinases in antigen-presenting cells. We studied the capacity of different antioxidants (ascorbic acid, alpha-tocopherol, pyrrolidine dithiocarbamate, N-acetylcysteine, and glutathione) to block the increase in tyrosine phosphorylation in human monocytes seen after stimulation with strong contact sensitizers. Human peripheral blood mononuclear cells were stimulated with 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone in the presence or absence of these antioxidants. The total amount of membrane-associated phosphotyrosine in CD14+ cells was quantifi…

Antigen-Presenting CellsDermatologyPicryl ChlorideDermatitis ContactBiochemistryAntioxidantschemistry.chemical_compoundPyrrolidine dithiocarbamateHumansdendritic cellsCysteineSulfhydryl CompoundsTyrosinePhosphorylationAntigen-presenting cellMolecular BiologyCells CulturedNF-kappa BTyrosine phosphorylationCell BiologyGlutathioneAscorbic acidGlutathioneAcetylcysteineMAP kinaseschemistryBiochemistrycontact sensitizerthiol antioxidantTyrosineSignal transductionMitogen-Activated Protein KinasesmonocytesCysteineThe Journal of investigative dermatology
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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Coupling of Contact Sensitizers to Thiol Groups is a Key Event for the Activation of Monocytes and Monocyte-Derived Dendritic Cells

2003

Strong contact sensitizers are able to induce distinct signal transduction mechanisms in antigen-presenting cells by coupling to cell proteins. The predominant target structures of haptens are thought to be thiol and amino groups in cysteine and lysine residues. We studied whether coupling of small reactive chemicals to thiol or amino groups might be responsible for the activation of monocytes and mature monocyte-derived dendritic cells. Human peripheral blood mononuclear cells were stimulated in vitro with subtoxic concentrations of the strong haptens 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone and 2, 4, 6-trinitrochlorobenzene, the thiol-reactive reagents N-hydroxymaleim…

MAP Kinase Signaling SystemCD14SuccinimidesPicryl ChlorideDermatologyAcetatesPeripheral blood mononuclear cellBiochemistryamino groupsAntioxidantsMonocytesMaleimideschemistry.chemical_compoundAnti-Infective AgentsmedicineHumansCysteineSulfhydryl CompoundsPhosphorylationAntigen-presenting cellMolecular Biologythiol groupsChemistryMonocyteLysineSulfhydryl ReagentsTyrosine phosphorylationDendritic cellDendritic CellsCell BiologyThiazolesmedicine.anatomical_structureBiochemistryEthylmaleimidehaptenTyrosineSignal transductionsignal transductionCysteineInterleukin-1Journal of Investigative Dermatology
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Impaired Th1 responses in mice deficient in Epstein-Barr virus-induced gene 3 and challenged with physiological doses of Leishmania major.

2005

Protection against Leishmania major is dependent on IL-12 release from L. major-infected dendritic cells (DC) that induce IFN-gamma-producing Th1/Tc1 cells. IL-27, a novel member of the IL-12 family, is a heterodimer composed of p28 and IL-12p40-related Epstein-Barr virus-induced gene 3 (EBI3), and was shown to be produced by DC. In this study, we utilized EBI3-deficient mice to investigate the role of IL-27 in leishmaniasis using physiological low-dose infections that mimic natural transmissions. Lesions in EBI3(-/-) mice were significantly larger between weeks 3 and 10 post infection, reaching up to approximately threefold increased lesion volumes compared to wild types. In parallel, derm…

ImmunologyPopulationCD11cLeishmaniasis CutaneousBiologyLesionMinor Histocompatibility AntigensMiceT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsLeishmania majorRNA MessengerReceptors CytokineeducationLeishmania majoreducation.field_of_studyEBI3Dendritic cellDendritic CellsTh1 Cellsbiology.organism_classificationImmunologyInterleukin 12Lymphmedicine.symptomEuropean journal of immunology
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Activation and translocation of p38 mitogen-activated protein kinase after stimulation of monocytes with contact sensitizers.

2002

Recently we described the induction of tyrosine phosphorylation by contact sensitizers as an early molecular event during the activation of antigen- presenting cells. In this study, the role of the p38 mitogen-activated protein kinase for the activation of human monocytes after exposure to four structurally unrelated contact sensitizers was analyzed in comparison with the irritant benzalkonium chloride and an inductor of oxidative stress (H 2 O 2 ) using immunofluorescence, Western blotting, and enzyme-linked immunosorbent assay techniques. Bio chemical analysis revealed a translocation of p38 from the cytoplasm to the detergent-resistant cell fraction only upon stimulation with contact sen…

CytoplasmMAP Kinase Signaling SystemPyridinesp38 mitogen-activated protein kinasesDermatologyBiologyIn Vitro TechniquesBiochemistryp38 Mitogen-Activated Protein KinasesMonocyteschemistry.chemical_compoundProto-Oncogene ProteinsHumansEnzyme InhibitorsPhosphorylationProtein kinase ATranscription factorMolecular Biologyets-Domain Protein Elk-1KinaseImidazolesTyrosine phosphorylationBiological TransportCell BiologyMolecular biologyDNA-Binding ProteinsEnzyme ActivationIL-1β/irritantchemistryhaptenMitogen-activated protein kinasebiology.proteinIrritantsPhosphorylationSignal transductionMitogen-Activated Protein KinasesBenzalkonium CompoundsHaptenssignal transductionInterleukin-1Transcription FactorsThe Journal of investigative dermatology
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Human primary dendritic cell subsets differ in their IL-12 release in response to Leishmania major infection

2010

Immunity against leishmaniasis has primarily been studied in experimental infections of mice. It was shown that infected skin dendritic cells (DC) are critical for the induction of protection against this pathogen, and targeting skin DC in vaccination approaches in mice has proven to be successful. However, little is known about the contribution of human DC subsets from the skin to primary immunity against this pathogen. In this study, we have analysed the interaction between different human DC subsets and Leishmania major. Primary human myeloid and monocyte-derived DC ingested the parasite comparable to that of murine skin DC, and this resulted in DC activation and IL-12 release, a cytokin…

Langerhans cellbiologymedicine.medical_treatmentDermatologyDendritic cellLeishmaniabiology.organism_classificationBiochemistryVaccinationmedicine.anatomical_structureCytokineImmunityImmunologymedicineInterleukin 12Leishmania majorMolecular BiologyExperimental Dermatology
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