Search results for "Adoptive Transfer"

showing 10 items of 65 documents

Identifying SARS‐CoV‐2 ‘memory’ NK cells from COVID‐19 convalescent donors for adoptive cell therapy

2021

Abstract COVID‐19 disease is the manifestation of syndrome coronavirus 2 (SARS‐CoV‐2) infection, which is causing a worldwide pandemic. This disease can lead to multiple and different symptoms, being lymphopenia associated with severity one of the most persistent. Natural killer cells (NK cells) are part of the innate immune system, being fighting against virus‐infected cells one of their key roles. In this study, we determined the phenotype of NK cells after COVID‐19 and the main characteristic of SARS‐CoV‐2‐specific‐like NK population in the blood of convalescent donors. CD57+ NKG2C+ phenotype in SARS‐CoV‐2 convalescent donors indicates the presence of ‘memory’/activated NK cells as it ha…

DrugAdultMaleCèl·lulesmedia_common.quotation_subjectImmunologyPopulationBlood DonorsDiseaseHuman leukocyte antigenNK cellsmedicine.disease_causeCell therapyCOVID‐19medicineImmunology and AllergyHumanseducationmedia_commonCoronaviruseducation.field_of_studyInnate immune systembusiness.industrySARS-CoV-2fungiCOVID-19ConvalescenceOriginal ArticlesMiddle AgedPhenotypeAdoptive TransferKIRHLAKiller Cells NaturalImmunologyOriginal ArticleFemalecell therapybusinessImmunologic MemoryImmunology
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L-Selectin-deficient SJL and C57BL/6 mice are not resistant to experimental autoimmune encephalomyelitis

2008

L-selectin has been suggested to play a role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Here we demonstrate that L-selectin(-/-) SJL mice are susceptible to proteolipid protein (PLP)-induced EAE because the compromised antigen-specific T cell proliferation in peripheral lymph nodes is fully compensated by the T cell response raised in their spleen. Transfer of PLP-specific T cells into syngeneic recipients induced EAE independent of the presence or absence of L-selectin on PLP-specific T cells or in the recipient. Leukocyte infiltration into the central nervous system parenchyma was detectable independent of the mode of dis…

Encephalomyelitis Autoimmune ExperimentalProteolipid protein 1OvalbuminT cellImmunologySpleenPathogenesisMice03 medical and health sciencesMyelin0302 clinical medicineCell Movementimmune system diseasesmedicineAnimalsImmunology and AllergyL-SelectinMyelin Proteolipid Protein030304 developmental biologyInflammation0303 health sciencesbiologyExperimental autoimmune encephalomyelitismedicine.diseaseAdoptive TransferOligodendrocytenervous system diseases3. Good healthMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinFemaleL-selectinSpleen030215 immunologyEuropean Journal of Immunology
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Lentivirus-induced dendritic cells for immunization against high-risk WT1(+) acute myeloid leukemia.

2013

Wilms' tumor 1 antigen (WT1) is overexpressed in acute myeloid leukemia (AML), a high-risk neoplasm warranting development of novel immunotherapeutic approaches. Unfortunately, clinical immunotherapeutic use of WT1 peptides against AML has been inconclusive. With the rationale of stimulating multiantigenic responses against WT1, we genetically programmed long-lasting dendritic cells capable of producing and processing endogenous WT1 epitopes. A tricistronic lentiviral vector co-expressing a truncated form of WT1 (lacking the DNA-binding domain), granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukin-4 (IL-4) was used to transduce human monocytes ex vivo. Overnight transd…

Genes Wilms TumorCell SurvivalGenetic VectorsAntineoplastic AgentsBiologyCD8-Positive T-LymphocytesLymphocyte ActivationPeripheral blood mononuclear cellEpitopeMonocytesViral vectorMiceAntigenRisk FactorsGeneticsmedicineNeoplasmAnimalsHumansMolecular BiologyResearch ArticlesOligonucleotide Array Sequence AnalysisCD86LentivirusGene Transfer TechniquesMyeloid leukemiaGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationDendritic CellsGenetic Therapymedicine.diseaseAdoptive TransferLeukemia Myeloid AcuteGene Expression RegulationCancer researchLeukocytes MononuclearMolecular MedicineInterleukin-4Ex vivoHuman gene therapy
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Cutting Edge: TGF-β Signaling Is Required for the In Vivo Expansion and Immunosuppressive Capacity of Regulatory CD4+CD25+ T Cells

2004

Abstract Data regarding the role of TGF-β for the in vivo function of regulatory CD4+CD25+ T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-β signaling specifically in T cells was used to assess the role of endogenous TGF-β for the in vivo function of CD4+CD25+ Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4+CD25+ Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4+CD25+ Treg we could demonstrate that endogenous TGF-β promotes the expansion of CD4+CD25+ Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4+CD25+ Treg and were …

Genetically modified mouseAdoptive cell transferTransgeneImmunologychemical and pharmacologic phenomenaEndogenyBiologyT-Lymphocytes RegulatoryMiceTransforming Growth Factor betaIn vivomedicineAnimalsHumansImmunology and AllergyGenetic Predisposition to DiseaseLymphocyte CountIL-2 receptorColitisReceptorCell DifferentiationReceptors Interleukin-2hemic and immune systemsColitismedicine.diseaseAdoptive TransferCell biologyImmunologySignal TransductionThe Journal of Immunology
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Severe hepatic injury in interleukin 18 (IL-18) transgenic mice: a key role for IL-18 in regulating hepatocyte apoptosis in vivo.

2004

Background: Interleukin 18 (IL-18) is a cytokine with pleiotropic activity that augments T helper 1 responses and cytotoxic activity of natural killer cells. Methods: To assess the function of IL-18 in vivo, we generated IL-18 transgenic (IL-18 Tg) mice under the control of a CD2 promoter/enhancer construct. Results: Macroscopically, IL-18 Tg mice showed reduced relative liver weight compared with wild-type littermates. TUNEL assays demonstrated increased hepatocyte apoptosis, and primary hepatocytes isolated from IL-18 Tg mice exhibited an increased spontaneous apoptosis rate. Furthermore, cross linking of Fas increased significantly the apoptosis rate in hepatocytes isolated from wild- ty…

Genetically modified mousemedicine.medical_specialtyTransgeneT-LymphocytesApoptosisMice TransgenicMice SCIDBiologyTransfectionTranslocation GeneticInterferon-gammaMiceIn vivoInternal medicinemedicineCytotoxic T cellAnimalsfas ReceptorL-SelectinCells CulturedLiver injuryTumor Necrosis Factor-alphaGastroenterologyInterleukin-18NF-kappa BOrgan Sizemedicine.diseaseAdoptive TransferEndocrinologymedicine.anatomical_structureLiverApoptosisHepatocyteLymphocyte TransfusionCancer researchHepatocytesInterleukin 18Gut
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Experimental Preemptive Immunotherapy of Murine Cytomegalovirus Disease with CD8 T-Cell Lines Specific for ppM83 and pM84, the Two Homologs of Human …

2001

ABSTRACTCD8 T cells are the principal antiviral effectors controlling cytomegalovirus (CMV) infection. For human CMV, the virion tegument protein ppUL83 (pp65) has been identified as a source of immunodominant peptides and is regarded as a candidate for cytoimmunotherapy and vaccination. Two sequence homologs of ppUL83 are known for murine CMV, namely the virion protein ppM83 (pp105) expressed late in the viral replication cycle and the nonstructural protein pM84 (p65) expressed in the early phase. Here we show that ppM83, unlike ppUL83, is not delivered into the antigen presentation pathway after virus penetration before or in absence of viral gene expression, while other virion proteins o…

Human cytomegalovirusMuromegalovirusmedicine.medical_treatmentImmunologyImmunodominanceCD8-Positive T-LymphocytesBiologyMicrobiologyCell LineViral Matrix ProteinsInterferon-gammaMiceImmune systemAntigenVirologyVaccines and Antiviral AgentsmedicineAnimalsCytotoxic T cellMice Inbred BALB CHerpesviridae InfectionsImmunotherapyPhosphoproteinsmedicine.diseaseAdoptive TransferVirologyPeptide FragmentsDisease Models AnimalViral replicationInsect ScienceImmunologyFemaleCytokine secretionImmunologic MemoryJournal of Virology
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Inhibition of murine IgE and immediate cutaneous hypersensitivity responses to ovalbumin by the immunomodulatory agent leflunomide

1999

SUMMARYLeflunomide has been identified as an immunoregulatory and anti-inflammatory compound. Allergic disease is characterized by elevated serum IgE levels, production of allergen-specific IgE and the release of inflammatory mediators from mast cells and granulocytes. Here we demonstrate, using an in vivo murine model, the ability of leflunomide to down-regulate levels of total and allergen-specific serum IgE production. Mice receiving leflunomide (45 mg/kg) orally at the time of primary immunization with ovalbumin adsorbed to aluminium hydroxide adjuvant, showed a reduction in total serum IgE levels of 95%, 41% and 32% following primary, secondary and tertiary immunizations, respectively …

Hypersensitivity ImmediateOvalbuminT-LymphocytesImmunologyPopulationDown-RegulationImmunoglobulin ESkin DiseasesMiceAdjuvants ImmunologicmedicineImmunology and AllergyAnimalseducationInterleukin 5Leflunomideeducation.field_of_studyMice Inbred BALB CbiologyVaccinationOriginal ArticlesIsoxazolesAllergensImmunoglobulin EAdoptive TransferTransplantationOvalbuminImmunoglobulin class switchingImmunologyAntibody Formationbiology.proteinFemaleAntibodyInterleukin-5Immunologic MemoryLeflunomidemedicine.drug
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A central role for Notch in effector CD8(+) T cell differentiation.

2014

Activated CD8(+) T cells choose between terminal effector cell (TEC) or memory precursor cell (MPC) fates. We found that the signaling receptor Notch controls this 'choice'. Notch promoted the differentiation of immediately protective TECs and was correspondingly required for the clearance of acute infection with influenza virus. Notch activated a major portion of the TEC-specific gene-expression program and suppressed the MPC-specific program. Expression of Notch was induced on naive CD8(+) T cells by inflammatory mediators and interleukin 2 (IL-2) via pathways dependent on the metabolic checkpoint kinase mTOR and the transcription factor T-bet. These pathways were subsequently amplified d…

ImmunologyNotch signaling pathwayMice TransgenicCell SeparationBiologyAdaptive ImmunityCD8-Positive T-LymphocytesEffector cellLymphocyte ActivationReal-Time Polymerase Chain ReactionArticlememoryMiceOrthomyxoviridae InfectionsCell surface receptorT-Lymphocyte SubsetsTransduction GeneticPrecursor cellImmunology and AllergyCytotoxic T cellAnimalsGeneticsReceptors NotchEffectorCell DifferentiationFlow CytometryAdoptive TransferTEC3. Good healthCell biologyMice Inbred C57BLeffectorCD8 T cellMPCInfluenza A virusinflammationTranscriptomeCD8Nature immunology
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Cannabinoid 1 Receptors in Keratinocytes Modulate Proinflammatory Chemokine Secretion and Attenuate Contact Allergic Inflammation

2013

Abstract Epidermal keratinocytes (KCs) and cannabinoid (CB) receptors both participate in the regulation of inflammatory responses in a mouse model for allergic contact dermatitis, the contact hypersensitivity (CHS) response to the obligate sensitizer 2,4-dinitrofluorobenzene. In this study, we investigated the cellular and molecular mechanisms how CB1 receptors attenuate CHS responses to 2,4-dinitrofluorobenzene. We used a conditional gene-targeting approach to identify the relative contribution of CB1 receptors on epidermal KCs for the control of CHS responses. To determine the underlying cellular and molecular mechanisms that regulate inflammatory responses in the effector phase of CHS, …

KeratinocytesChemokineImmunologyInflammationStimulationBiologyProinflammatory cytokineAllergic inflammationInterferon-gammaMiceReceptor Cannabinoid CB1medicineAnimalsChemokine CCL8Immunology and AllergyCXCL10ReceptorCells CulturedCell ProliferationInflammationMice Knockoutintegumentary systemEarAdoptive TransferChemokine CXCL10Mice Inbred C57BLDermatitis Allergic ContactImmunologyChemokine secretionbiology.proteinDinitrofluorobenzenemedicine.symptomThe Journal of Immunology
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Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

2013

SummaryLiver fibrosis is a consequence of chronic liver diseases and thus a major cause of mortality and morbidity. Clinical evidence and animal studies suggest that local tissue homeostasis is disturbed due to immunological responses to chronic hepatocellular stress. Poorly defined stress-associated inflammatory networks are thought to mediate gradual accumulation of extracellular-matrix components, ultimately leading to fibrosis and liver failure. Here we have reported that hepatic expression of interleukin-33 (IL-33) was both required and sufficient for severe hepatic fibrosis in vivo. We have demonstrated that IL-33’s profibrotic effects related to activation and expansion of liver resi…

Liver CirrhosisLiver cytologyImmunologyBiologyLymphocyte ActivationArticle03 medical and health sciencesMice0302 clinical medicineFibrosismedicineHepatic Stellate CellsAnimalsImmunology and AllergyLymphocytesReceptors Interleukin-4 Type IIInterleukin 4Tissue homeostasisCells Cultured030304 developmental biologyCell ProliferationInflammationMice Knockout0303 health sciencesMice Inbred BALB CInterleukin-13InterleukinsInnate lymphoid cellmedicine.diseaseInterleukin-33Adoptive Transfer3. Good healthInterleukin 33Mice Inbred C57BLInfectious DiseasesLiverImmunologyHepatic stellate cellHepatic fibrosisSTAT6 Transcription Factor030215 immunologySignal TransductionImmunity
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