Search results for " Helper-Inducer"

showing 10 items of 81 documents

Combining dasatinib with dexamethasone long-term leads to maintenance of antiviral and antileukemia specific cytotoxic T cell responses in vitro

2012

Maintaining graft versus leukemia (GvL) and antivirus responses of cytotoxic T cells (CTLs) while suppressing graft-versus-host disease (GvHD) remains a challenge after allogeneic bone marrow transplantation. Clinical observations indicate that combining glucocorticoids with multi-tyrosine-kinase inhibitors could be a successful therapeutic approach. We and others have shown that the BCR-ABL/SRC kinase inhibitor dasatinib may enhance or suppress T cells in vitro. In this report, we evaluated combination effects of dasatinib and dexamethasone on CD3 + and virus-specific CD8 + T cells directly ex vivo and on antigen-specific leukemia-reactive and alloreactive CD8 + T cell clones. Functional o…

Cytotoxicity ImmunologicHerpesvirus 4 HumanCancer ResearchNaive T cellT cellDasatinibDrug Evaluation PreclinicalReceptors Antigen T-CellCytomegalovirusApoptosisT-Cell Antigen Receptor SpecificityBiologyLymphocyte ActivationCell DegranulationDexamethasoneAntigenHLA AntigensT-Lymphocyte SubsetsGeneticsmedicineHumansCytotoxic T cellAntigens ViralProtein Kinase InhibitorsMolecular BiologyCells CulturedDegranulationDrug SynergismT-Lymphocytes Helper-InducerCell BiologyHematologyDasatinibThiazolesPyrimidinesmedicine.anatomical_structureImmunologyCancer researchCytokinesK562 CellsMemory T cellCell DivisionCD8Signal TransductionT-Lymphocytes Cytotoxicmedicine.drugExperimental Hematology
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H-2(d) mice born to and reared by HBeAg-transgenic mothers do not develop T cell tolerance toward the hepatitis B virus core gene products.

2000

The function of the secretory core gene product (HBeAg) of the human hepatitis B virus (HBV) is unknown. It has been proposed that this protein may be passed from the mother to her offspring at the perinatal stage where it might induce immune tolerance. In a previous study we have shown that the murine placenta presents an efficient barrier for the HBe protein and that H-2(b) mice born to HBeAg-positive transgenic mothers do not develop tolerance of specific cytotoxic T cells. In the present work we demonstrate that transgenic mice expressing high serum levels of HBeAg secrete only small amounts of this protein into their milk and excrete minute amounts of the viral gene product in their ur…

Cytotoxicity ImmunologicMaleHepatitis B virusT cellvirusesT-LymphocytesMothersMice TransgenicBiologymedicine.disease_causeLymphocyte ActivationImmune toleranceMiceImmune systemVirologymedicineImmune ToleranceCytotoxic T cellAnimalsHepatitis B e AntigensHepatitis B AntibodiesHepatitis B virusMice Inbred BALB CH-2 Antigensvirus diseasesT-Lymphocytes Helper-InducerHepatitis Bmedicine.diseaseHepatitis BVirologydigestive system diseasesPeptide Fragmentsmedicine.anatomical_structureMilkHBeAgAnimals NewbornImmunologyFemaleCD8T-Lymphocytes CytotoxicVirology
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma.

2007

T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of ROR alpha promoted Th17 differentiation, possibly through the c…

Encephalomyelitis Autoimmune ExperimentalReceptors Retinoic AcidT cellImmunologyRetinoic acidReceptors Cytoplasmic and NuclearElectrophoretic Mobility Shift AssayBiology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineT-Lymphocyte SubsetsmedicineT helper 17 cellImmunology and AllergyAnimalsCell LineageReceptorMOLIMMUNOTranscription factor030304 developmental biologyOrphan receptor0303 health sciencesReceptors Thyroid HormoneReverse Transcriptase Polymerase Chain ReactionInterleukin-17Cell DifferentiationNuclear Receptor Subfamily 1 Group F Member 1T-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyMice Mutant StrainsCell biologymedicine.anatomical_structureInfectious DiseaseschemistryNuclear receptorSTAT proteinTrans-ActivatorsFemale030215 immunologyImmunity
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The protein tyrosine kinase Tec regulates a CD44highCD62L- Th17 subset.

2010

Abstract The generation of Th17 cells has to be tightly controlled during an immune response. In this study, we report an increase in a CD44highCD62L− Th17 subset in mice deficient for the protein tyrosine kinase Tec. CD44highCD62L− Tec−/− CD4+ T cells produced enhanced IL-17 upon activation, showed increased expression levels of IL-23R and RORγt, and IL-23–mediated expansion of Tec−/− CD4+ T cells led to an increased production of IL-17. Tec−/− mice immunized with heat-killed Streptococcus pneumoniae displayed increased IL-17 expression levels in the lung postinfection with S. pneumoniae, and this correlated with enhanced pneumococcal clearance and reduced lung inflammation compared with T…

Encephalomyelitis Autoimmune ExperimentalTECeducationImmunologyImmunoblottingInflammationEnzyme-Linked Immunosorbent AssayCell SeparationBiologyMiceImmune systemIn vivoRAR-related orphan receptor gammaT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsCell LineageL-SelectinMice KnockoutReverse Transcriptase Polymerase Chain ReactionCD44Interleukin-17hemic and immune systemsCell DifferentiationPneumoniaT-Lymphocytes Helper-InducerProtein-Tyrosine KinasesFlow CytometryMolecular biologyHyaluronan ReceptorsCancer researchbiology.proteinCytokinesmedicine.symptomSignal transductiontissuesTyrosine kinaseSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+regulatory T cells

2008

The conditions leading to the induction of adaptive Foxp3+regulatory T cells (T-regs) from peripheral T cells in vivo are incompletely understood. Here, we show that unresponsiveness of T cells to IL-6 by T cell-selective deletion of gp130 or immunization of wild-type mice with antigen in incomplete Freund's adjuvant (IFA), which fails to induce IL-6, promotes the conversion of peripheral CD4+T cells into adaptive Foxp3+T-regs. Thus, both T cell-conditional gp130 knockout (KO) mice immunized with MOG35-55 in complete Freund's adjuvant (CFA) and wild-type mice immunized with MOG35-55 in IFA develop overwhelming antigen-specific T-reg responses and are protected from experimental autoimmune e…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentchemical and pharmacologic phenomenaInflammationBiologyT-Lymphocytes RegulatoryMiceInterleukin 21Antigenimmune system diseasesmedicineAnimalsCytotoxic T cellIL-2 receptorMice KnockoutMultidisciplinaryInterleukin-6Experimental autoimmune encephalomyelitisFOXP3Forkhead Transcription Factorshemic and immune systemsT-Lymphocytes Helper-InducerBiological Sciencesmedicine.diseaseCytokineImmunologymedicine.symptomProceedings of the National Academy of Sciences
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Hepatitis C virus antibody secretion in vitro by peripheral blood lymphocytes.

1992

A recombinant polypeptide corresponding to a virus-specific cDNA clone (c100-3) serves as the antigen for a hepatitis C virus (HCV) antibody assay. Previous investigations have shown an 80% prevalence of HCV antibodies in sera of patients suffering from post-transfusional chronic hepatitis non-A, non-B, but positive results were also obtained for 30 to 70% of sera from patients with chronic hepatitis B or autoimmune hepatitis. In this study we show that HCV antibodies are secreted by peripheral blood lymphocytes (PBL) in vitro. PBL from 12/35 patients with chronic non-A, non-B hepatitis and 1/6 patients with chronic active hepatitis B spontaneously secreted HCV antibodies in cell culture su…

Hepatitis C virusT-LymphocytesEnzyme-Linked Immunosorbent AssayAutoimmune hepatitisHepacivirusBiologymedicine.disease_causeLymphocyte ActivationVirusAntigenmedicineHumansHepatitis AntibodiesLymphocytesHepatitisB-LymphocytesHepatologyvirus diseasesT-Lymphocytes Helper-Inducermedicine.diseaseVirologydigestive system diseasesPolyclonal antibodiesHumoral immunityImmunologybiology.proteinAntibodyJournal of hepatology
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Lymphokine profile and activation pattern of two unrelated antigen- or idiotype-specific T suppressor cell clones.

1992

Two T suppressor (Ts) clones of different specificity have been analyzed for their lymphokine spectrum. BVI/5 is an I-Ek-restricted bovine serum albumin (BSA)-specific Ts cell clone from a CBA/J mouse tolerized by low doses of BSA. It affects directly or indirectly the function of BSA-specific T helper (Th) cells. The Ts cell clone 178-4 from a BALB/c mouse is I-Ed restricted and recognizes the public J558 Id on B cells. It prevents alpha(1----3)dextran B 1355S (Dex)-specific IgG antibody production and drives Dex-specific J558 idiotype-bearing B cells into an anergic B IgG memory cell state. Both Ts cell clones thus cause specific suppression, yet in different experimental systems using di…

IdiotypeMalemedicine.medical_treatmentImmunologyLymphocyte ActivationT-Lymphocytes RegulatoryInterferon-gammaMiceAntigenInterferonAntibody SpecificityCell ClonemedicineImmunology and AllergyAnimalsAntigensLymphokinesCD40biologyLymphokineHistocompatibility Antigens Class IISerum Albumin BovineT-Lymphocytes Helper-InducerMolecular biologyClone CellsCytokineImmunologybiology.proteinMice Inbred CBAClone (B-cell biology)medicine.drugInterleukin-1European journal of immunology
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Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

2011

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have ena…

Immunity Cellular/geneticsCellular immunityMultiple SclerosisGenome-wide association studyCLEC16ABiologyPolymorphism Single NucleotideCell Differentiation/immunologyEurope/ethnologyMajor Histocompatibility Complex/geneticsMajor Histocompatibility Complex03 medical and health sciences0302 clinical medicinemedicineGenetic predispositionHumansGenetic Predisposition to DiseaseHLA-A Antigens/geneticsAlleles030304 developmental biologyGenetic associationGenetics0303 health sciencesImmunity CellularMultidisciplinaryHLA-A AntigensGenome HumanMultiple sclerosisGenetic Predisposition to Disease/geneticsHLA-DR Antigens/geneticsLymphocyte differentiationCell DifferentiationHLA-DR AntigensT-Lymphocytes Helper-InducerRC346medicine.diseasePolymorphism Single Nucleotide/geneticsGenetic architecture3. Good healthEuropeSample SizeImmunologyGenome Human/geneticsMultiple Sclerosis/genetics030217 neurology & neurosurgeryT-Lymphocytes Helper-Inducer/cytologyGenome-Wide Association StudyHLA-DRB1 Chains
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Interferon-regulatory factor 4 is essential for the developmental program of T helper 9 cells.

2010

Summary Interferon-regulatory factor 4 (IRF4) is essential for the development of T helper 2 (Th2) and Th17 cells. Herein, we report that IRF4 is also crucial for the development and function of an interleukin-9 (IL-9)-producing CD4 + T cell subset designated Th9. IRF4-deficient CD4 + T cells failed to develop into IL-9-producing Th9 cells, and IRF4-specific siRNA inhibited IL-9 production in wild-type CD4 + T cells. Chromatin-immunoprecipitation (ChIP) analyses revealed direct IRF4 binding to the Il9 promoter in Th9 cells. In a Th9-dependent asthma model, neutralization of IL-9 substantially ameliorated asthma symptoms. The relevance of these findings is emphasized by the fact that the ind…

ImmunologyBiologyPathogenesisInterleukin 21MiceDownregulation and upregulationmedicineImmunology and AllergyAnimalsHumansInterleukin 9RNA Small InterferingMOLIMMUNOPromoter Regions GeneticCells CulturedMice KnockoutInterleukin-9Cell DifferentiationT helper cellT-Lymphocytes Helper-InducerAsthmaMice Inbred C57BLInfectious Diseasesmedicine.anatomical_structureCELLIMMUNOImmunologyInterferon Regulatory FactorsFunction (biology)Platelet factor 4IRF4Protein BindingImmunity
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