Search results for "Th2 Cells"

showing 10 items of 98 documents

M2 Polarized Macrophages and Giant Cells Contribute to Myofibrosis in Neuromuscular Sarcoidosis

2011

The etiopathogenesis of sarcoidosis, a systemic granulomatous disease, still remains obscure. A multitude of organs have been described to be affected in systemic sarcoidosis. Skeletal muscles may also be affected, leading to myalgia and weakness. A workup of the specific immune response with emphasis on the macrophage response is provided herein. Affected muscle tissue from seven patients with systemic sarcoidosis was analyzed and compared with that from seven patients with other myopathies containing macrophagocytic infiltration. Monocytes/macrophages and giant cells in granulomas of muscle tissue from patients with sarcoidosis show a status of alternative activation (M2) based on their e…

MalePathologymedicine.medical_specialtySystemic diseaseSarcoidosismedicine.medical_treatmentBiologyGiant CellsMonocytesPathology and Forensic MedicineTh2 CellsImmune systemmedicineHumansMacrophageRNA MessengerMuscle SkeletalAgedGranulomaMacrophagesCCL18Cell PolarityEpithelial CellsRegular ArticleNeuromuscular DiseasesMacrophage ActivationMiddle Agedmedicine.diseaseAcquired immune systemFibrosisPhenotypeCytokineGene Expression RegulationGiant cellChemokines CCGranulomaImmunologyCytokinesFemaleThe American Journal of Pathology
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N-3 fatty acids modulate Th1 and Th2 dichotomy in diabetic pregnancy and macrosomia.

2006

We assessed the implication of Th (helper)-cells and the modulation of the Th1/Th2 dichotomy by n-3 polyunsaturated fatty acids (PUFA) in type I diabetic pregnancy (DP) and macrosomia. Female gestant rats fed a standard diet or n-3 PUFA regimen were rendered diabetic by administration of five low doses of streptozotocin. The macrosomic (MAC) offspring were sacrificed at the age of 90 days. The mRNAs of IL-2 and IFN-gamma (Th1 cytokines) and IL-4 (Th2 cytokine) were downregulated in the pancreas and spleen of diabetic pregnant rats. The levels of IL-10 mRNA, another Th2 cytokine, were unchanged in the spleen or upregulated in the pancreas of these animals. Feeding an n-3 PUFA diet to rats wi…

Malemedicine.medical_specialtyOffspringImmunologyPregnancy in DiabeticsSpleenBiologyFetal MacrosomiaTh2 CellsDownregulation and upregulationPregnancyInternal medicineDiabetes mellitusFatty Acids Omega-3medicineImmunology and AllergyAnimalsRNA MessengerRats Wistarchemistry.chemical_classificationPregnancyFatty AcidsTh1 CellsStreptozotocinmedicine.diseaseDietRatsmedicine.anatomical_structureEndocrinologyCholesterolDiabetes Mellitus Type 1chemistryCytokinesFemalePancreasSpleenmedicine.drugPolyunsaturated fatty acidJournal of autoimmunity
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T-bet as a possible therapeutic target in autoimmune disease

2002

The prominent role of pro-inflammatory cytokines produced by T helper-1 (T(H1)) cells in regulating autoimmune responses in vitro and in vivo has been demonstrated. Recent observations of T cell polarisation by regulatory transcription factors--especially T-bet (T-box expressed in T cells)--raise the question of their influence in controlling autoimmune diseases. Here, the authors summarise recent observations of the role of T-bet in controlling chronic inflammatory and autoimmune diseases and discuss the implications of these findings for future therapeutic approaches.

Mice Inbred MRL lprTranscription GeneticTransgeneT cellCellular differentiationClinical BiochemistryMice TransgenicLymphocyte ActivationAutoimmune DiseasesInterferon-gammaMiceTh2 CellsCrohn DiseaseDrug DiscoverymedicineAnimalsLupus Erythematosus SystemicIL-2 receptorIntestinal MucosaMice KnockoutPharmacologyAutoimmune diseaseLupus erythematosusbusiness.industryZAP70Cell DifferentiationTh1 CellsColitisInflammatory Bowel Diseasesmedicine.diseaseCeliac DiseaseDisease Models Animalmedicine.anatomical_structureCTLA-4ImmunologyCytokinesMolecular MedicineT-Box Domain ProteinsbusinessTranscription FactorsExpert Opinion on Therapeutic Targets
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Increased immunosuppressive function of CD4(+)CD25(+)Foxp3(+)GITR+ T regulatory cells from NFATc2((-/-)) mice controls allergen-induced experimental …

2012

The expansion of effector T cells is tightly controlled by transcription factors like nuclear factor of activated T cells (NFAT) family members that mediate early intracellular responses to T cell receptor-mediated signals. In this study we show that, after allergen challenge, NFATc2((-/-)) mice had augmented number of functionally intact CD4(+)CD25(++)GITR(++) T regulatory (T regs) cells in the lung. Anti-GITR antibody treatment inhibited T regulatory cell function and enhanced the number of activated lung CD4(+) T cells associated with increased IL-2 and pSTAT-5 in the airways of NFATc2((-/-)) mice in experimental allergic asthma. This agonistic treatment led to increased inflammation in …

NFATC2T cellImmunologyInflammationBiologyT-Lymphocytes RegulatoryInterleukin 21MiceTh2 CellsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyAnimalsIL-2 receptorLungImmunosuppression TherapyMice KnockoutNFATC Transcription FactorsInterleukin-2 Receptor alpha SubunitFOXP3NFATForkhead Transcription FactorsHematologyAllergensAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinCytokinesTh17 CellsFemalemedicine.symptomAntibodySpleenImmunobiology
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Non-eosinophilic Airway Hyper-reactivity in Mice, Induced by IFN-γProducing CD4+and CD8+Lung T cells, is Responsive to Steroid Treatment

2014

Non-eosinophilic asthma is characterized by infiltration of neutrophils into the lung and variable responsiveness to glucocorticoids. The pathophysiological mechanisms have not been characterized in detail. Here, we present an experimental asthma model in mice associated with non-eosinophilic airway inflammation and airway hyper-responsiveness (AHR). For this, BALB/c mice were sensitized by biolistic DNA immunization with a plasmid encoding the model antigen β-galactosidase (pFascin-βGal mice). For comparison, eosinophilic airway inflammation was induced by subcutaneous injection of βGal protein (βGal mice). Intranasal challenge of mice in both groups induced AHR to a comparable extent as w…

NeutrophilsImmunologyInflammationBiologyLymphocyte ActivationDexamethasoneLymphocyte DepletionInterferon-gammaMiceTh2 CellsAntigenmedicineAnimalsLungDexamethasoneMice Inbred BALB CLungDNAGeneral MedicineBiolisticsTh1 Cellsrespiratory systembeta-Galactosidasemedicine.diseaseAsthmaNeutrophiliarespiratory tract diseasesEosinophilsDisease Models Animalmedicine.anatomical_structureNeutrophil InfiltrationImmunologyTh17 CellsFemaleGoblet Cellsmedicine.symptomBronchoalveolar Lavage FluidInfiltration (medical)CD8GlucocorticoidT-Lymphocytes Cytotoxicmedicine.drugScandinavian Journal of Immunology
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IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.

2009

Abstract Resistance to leishmaniasis in C57BL/6 mice depends on Th1/Tc1 cells. BALB/c mice preferentially develop Th2 immunity and succumb to infection. We now assessed the role of IL-17 in cutaneous leishmaniasis. During the course of Leishmania major infection, BALB/c CD4 cells and neutrophils produced increased amounts of IL-17 as compared with cells from C57BL/6 mice. This increase was associated with significantly increased IL-23 release from L. major-infected BALB/c dendritic cells (DC), whereas IL-6 and TGF-β1 production by BALB/c and C57BL/6 DC were comparable. Interestingly, lesion sizes in infected IL-17-deficient BALB/c mice were dramatically smaller and failed to progress as com…

NeutrophilsImmunologyLeishmaniasis CutaneousBiologyInterleukin-23ArticleLesionMiceImmune systemTh2 CellsCutaneous leishmaniasisSpecies SpecificityImmunitymedicineImmunology and AllergyAnimalsLeishmania majorGenetic Predisposition to DiseaseInterleukin 4Cells CulturedLeishmania majorMice KnockoutImmunity CellularMice Inbred BALB CInterleukin-17Cell DifferentiationDendritic Cellsmedicine.diseasebiology.organism_classificationUp-RegulationMice Inbred C57BLInterleukin 10ImmunologyDisease ProgressionInterleukin 17medicine.symptomJournal of immunology (Baltimore, Md. : 1950)
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Signals involved in the early TH1/TH2 polarization of an immune response depending on the type of antigen.

1999

Abstract Background: The early production of distinct cytokines by epidermal cells (ECs) in response to antigen exposure may govern the development of T H1 -like immune responses, such as contact sensitivity, or T H2 -like immune responses, such as IgE-dependent allergies of the immediate type, depending on the type of antigen. Objective: The aim of this study was to compare the signals induced by protein allergens with those induced by haptens in ECs and subsequently in local draining lymph node cells (LNCs) or splenocytes. Methods: BALB/c mice were primed in vivo with the protein allergens ovalbumin or birch pollen or the haptens 2,4-dinitrofluorobenzene or trinitrochlorbenzene, respectiv…

Ovalbuminmedicine.medical_treatmentImmunologyImmunoglobulinsEnzyme-Linked Immunosorbent AssayPicryl ChlorideBiologyMiceImmune systemTh2 CellsAntigenmedicineDinitrochlorobenzeneImmunology and AllergyAnimalsRNA MessengerCells CulturedMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionCell PolarityEpithelial CellsT lymphocyteAllergensTh1 CellsInterleukin-10Interleukin 10OvalbuminBlotting SouthernKineticsCytokineImmunologybiology.proteinCytokinesPollenFemaleLymph NodesAntibodyHaptenHaptensSpleenSignal TransductionThe Journal of allergy and clinical immunology
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Epithelial-mesenchymal communication in the pathogenesis of chronic asthma.

2005

Although Th-2-mediated inflammation is a key therapeutic target in asthma, its relationship to altered structure and functions of the airways is largely unknown. In addition to inflammation, asthma is a disorder involving the airway epithelium that is more vulnerable to environmental injury and responds to this by impaired healing. This establishes a chronic wound scenario that is capable of sustaining chronic inflammation as well as remodeling. This response occurs as a consequence of activation of the epithelial-mesenchymal unit, involving reciprocal activities of growth factors belonging to the fibroblast growth factor, epidermal growth factor, and transforming growth factor-beta familie…

Pulmonary and Respiratory MedicineChronic woundInflammationBiologyFibroblast growth factorPathogenesisTh2 CellsEpidermal growth factormedicineHumansGrowth Substancesasthma InflammationAsthmaInflammationWound HealingMesenchymal stem cellModels ImmunologicalEpithelial CellsMuscle SmoothFibroblastsmedicine.diseaseAsthmarespiratory tract diseasesImmunologyChronic DiseaseRespiratory Physiological PhenomenaRespiratory epitheliumCytokinesmedicine.symptom
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Divergent effects of biolistic gene transfer in a mouse model of allergic airway inflammation.

2007

Particle-mediated epidermal delivery (PMED) of allergen genes efficiently prevents systemic sensitization and suppresses specific immunoglobulin E synthesis. We investigated in a mouse model of allergic airway disease the effect of PMED on the elicitation of local inflammatory reactions in the lung. BALB/c mice were biolistically transfected with plasmids encoding beta-galactosidase (betaGal) as model allergen under control of the DC-targeting fascin promoter and the ubiquitously active cytomegalovirus promoter, respectively. Mice were challenged intranasally with betaGal-protein with or without intermediate sensitization with betaGal adsorbed to aluminiumhydroxide. Subsequently, local cyto…

Pulmonary and Respiratory Medicinemedicine.medical_treatmentClinical BiochemistryCytomegalovirusBiologymedicine.disease_causeDNA vaccinationInterferon-gammaMiceAllergenTh2 CellsmedicineRespiratory HypersensitivityAnimalsHumansPromoter Regions GeneticMolecular BiologyLungSensitizationCells CulturedInflammationMice Inbred BALB Cmedicine.diagnostic_testMicrofilament ProteinsGene Transfer TechniquesCell BiologyTransfectionDendritic Cellsrespiratory systemImmunoglobulin ETh1 Cellsmedicine.diseasebeta-Galactosidaserespiratory tract diseasesCellular infiltrationDisease Models Animalmedicine.anatomical_structureBronchoalveolar lavageCytokineNeutrophil InfiltrationImmunologyAntibody FormationFemaleEpidermisCarrier ProteinsBronchoalveolar Lavage FluidCD8T-Lymphocytes CytotoxicAmerican journal of respiratory cell and molecular biology
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Cyclic AMP-induced Chromatin Changes Support the NFATc-mediated Recruitment of GATA-3 to the Interleukin 5 Promoter

2008

Elevated intracellular cyclic AMP levels, which suppress the proliferation of naive T cells and type 1 T helper (Th1) cells are a property of T helper 2 (Th2) cells and regulatory T cells. While cyclic AMP signals interfere with the IL-2 promoter induction, they support the induction of Th2-type genes, in particular of il-5 gene. We show here that cyclic AMP signals support the generation of three inducible DNase I hypersensitive chromatin sites over the il-5 locus, including its promoter region. In addition, cyclic AMP signals enhance histone H3 acetylation at the IL-5 promoter and the concerted binding of GATA-3 and NFATc to the promoter. This is facilitated by direct protein-protein inte…

Quantitative Trait LociGATA3 Transcription FactorBiologyBiochemistryCell LineHistonesMiceTh2 CellsCyclic AMPTranscriptional regulationAnimalsHumansTranscription Chromatin and EpigeneticsPromoter Regions GeneticHistone H3 acetylationMolecular BiologyInterleukin 5Cell ProliferationMice Inbred BALB CNFATC Transcription FactorsEffectorLymphokineAcetylationZinc FingersPromoterCell BiologyDNA-binding domainTh1 CellsChromatin Assembly and DisassemblyMolecular biologyChromatinProtein Structure TertiaryChromatinGene Expression RegulationInterleukin-2Interleukin-5Signal TransductionJournal of Biological Chemistry
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