0000000000639435

AUTHOR

Jiirgen Knop

showing 4 related works from this author

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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Kontaktallergie (V 58–V 65)

2000

medicine.medical_specialtyOtorhinolaryngologybusiness.industrymedicineImmunology and AllergybusinessDermatologyAllergo Journal
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Infectious Tolerance

2002

Regulatory CD4(+)CD25(+) T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact-mediated suppression of conventional CD4(+) T cells by human CD25(+) Treg cells is fixation resistant, independent from membrane-bound TGF-beta but requires activation and protein synthesis of CD25(+) Treg cells. Coactivation of CD25(+) Treg cells with Treg cell-depleted CD4(+) T cells results in anergized CD4(+) T cells that in turn inhibit the activation of conventional, freshly isolated CD4(+) T helper (Th) cells. This infectious suppressive activity, transferred from CD25(+) Treg cells via cell contact, is cell contact-independent and partially medi…

TGF-βCD4-Positive T-Lymphocyteshuman regulatory T cellsT-LymphocytesImmunologyCellchemical and pharmacologic phenomenaIn Vitro TechniquesLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterleukin 21AntigenTransforming Growth Factor betaCD4+CD25+ T cellsCell AdhesionImmune TolerancemedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorbiologyBrief Definitive ReportModels ImmunologicalReceptors Interleukin-2hemic and immune systemsT-Lymphocytes Helper-InducerTransforming growth factor betainfectious tolerancemedicine.anatomical_structureT cell inhibitionImmunologyCancer researchbiology.proteinTransforming growth factorJournal of Experimental Medicine
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Regulatory activity of human CD4 CD25 T cells depends on allergen concentration, type of allergen and atopy status of the donor.

2005

Regulatory CD4+ CD25+ FoxP3-positive T cells (Treg) are functional in most atopic patients with allergic rhinitis and are able to inhibit T helper type 1 (Th1) and Th2 cytokine production of CD4+ CD25- T cells. This study was designed to analyse the following additional aspects: influence of allergen concentration, influence of the type of allergen, and influence of the atopy status of the donor on the strength of the regulatory activity. CD4+ CD25- T cells from healthy non-atopic controls or from grass-pollen-allergic or wasp-venom-allergic donors were stimulated alone or in the presence of Treg with autologous mature monocyte-derived dendritic cells which were pulsed with different concen…

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergymedicine.medical_treatmentImmunologyDose-Response Relationship Immunologicchemical and pharmacologic phenomenaWasp VenomsReceptors Nerve Growth FactorBiologymedicine.disease_causePoaceaeReceptors Tumor Necrosis FactorAtopyInterleukin 21AllergenTh2 CellsAntigenT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyHumansIL-2 receptorReceptorCells CulturedCell Proliferationhemic and immune systemsForkhead Transcription FactorsReceptors Interleukin-2Original ArticlesAllergensTh1 Cellsmedicine.diseaseCoculture TechniquesCytokineImmunologyCytokinesPollenImmunology
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