Search results for "Knockout"

showing 10 items of 806 documents

Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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CB(1) signaling in forebrain and sympathetic neurons is a key determinant of endocannabinoid actions on energy balance

2010

The endocannabinoid system (ECS) plays a critical role in obesity development. The pharmacological blockade of cannabinoid receptor type 1 (CB(1)) has been shown to reduce body weight and to alleviate obesity-related metabolic disorders. An unsolved question is at which anatomical level CB(1) modulates energy balance and the mechanisms involved in its action. Here, we demonstrate that CB(1) receptors expressed in forebrain and sympathetic neurons play a key role in the pathophysiological development of diet-induced obesity. Conditional mutant mice lacking CB(1) expression in neurons known to control energy balance, but not in nonneuronal peripheral organs, displayed a lean phenotype and res…

Sympathetic Nervous SystemPhysiologymedicine.medical_treatmentHUMDISEASEFluorescent Antibody TechniqueBody TemperatureMice0302 clinical medicineReceptor Cannabinoid CB1Cannabinoid receptor type 1ReceptorIn Situ HybridizationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionCB(1)ThermogenesisEndocannabinoid systemOBESITYCB1 knock outlipids (amino acids peptides and proteins)CB(1); CANNABINOID RECEPTOR; OBESITY; ENDOCANNABINOID SYSTEM; METABOLIC DISORDERSSignal Transductionmedicine.medical_specialtyforebrainImmunoblottingCitrate (si)-SynthaseIn situ hybridizationHyperphagiaBiologyDNA MitochondrialModels BiologicalENDOCANNABINOID SYSTEMMOLNEURONO03 medical and health sciencesProsencephalonLipid oxidationInternal medicineMETABOLIC DISORDERSmedicineAnimalsMolecular BiologyCANNABINOID RECEPTOR030304 developmental biologyAnalysis of VarianceX-Ray MicrotomographyCell Biologyendocannabinoidenergy balanceEndocrinologynervous systemsympathetic neuronsForebrainCannabinoidEnergy Metabolismendocannabinoid; forebrain; sympathetic neurons; energy balance; CB1 knock outNeuroscienceThermogenesis030217 neurology & neurosurgery
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Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein.

2010

Although generally considered a prototypical movement disorder, Parkinson's disease is commonly associated with a broad-spectrum of non-motor symptoms, including autonomic dysfunctions caused by significant alterations in catecholaminergic neurons of the peripheral sympathetic nervous system. Here we present evidence that alpha-synuclein is highly expressed by sympathetic ganglion neurons throughout embryonic and postnatal life and that it is found in tyrosine hydroxylase-positive sympathetic fibers innervating the heart of adult mice. However, mice deficient in alpha-synuclein do not exhibit any apparent alterations in sympathetic development. Sympathetic neurons isolated from mouse embryo…

Sympathetic nervous system1-Methyl-4-phenylpyridiniumα-Synuclein knockoutTyrosine 3-MonooxygenaseNeurotoxinsNeurotrophic factorSubstantia nigraBiologylcsh:RC321-571chemistry.chemical_compoundMiceCatecholaminesSympathetic Fibers PostganglionicParkinsonian DisordersNeurotrophic factorsmedicineNeurotoxinAutonomic gangliaAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCells CulturedNeuronsGanglia SympatheticCell DeathMPTPSympathetic ganglionMice Mutant Strainsnervous system diseasesMPP+medicine.anatomical_structureNeurologychemistrynervous system1-Methyl-4-phenyl-1236-tetrahydropyridinePeripheral nervous systemSympathetic nervous systemNerve Degenerationalpha-SynucleinCatecholaminergic cell groupsPeripheral nervous systemNeuroscienceNeurobiology of disease
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IL-23 receptor regulates unconventional IL-17-producing T cells that control bacterial infections.

2010

AbstractIL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of γδ and double negative (DN) αβ T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-γ, and TNF-α. Notably, DN T cells transferred into L. monocytogenes-infected RAG2−/− mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that …

T cellCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologyMice NudeMice TransgenicBiologyArticleImmunophenotypingInterferon-gammaMiceImmune systemAntigenCell MovementT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsInterferon gammaListeriosisCells CulturedMice KnockoutEffectorTumor Necrosis Factor-alphaIntracellular parasiteInterleukin-17Receptors Antigen T-Cell gamma-deltaReceptors InterleukinCoculture TechniquesCell biologymedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-23 Subunit p19Tumor necrosis factor alphaInterleukin 17Peritoneummedicine.drugJournal of immunology (Baltimore, Md. : 1950)
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Uptake of Leishmania major by dendritic cells is mediated by Fcγ receptors and facilitates acquisition of protective immunity

2006

Uptake of Leishmania major by dendritic cells (DCs) results in activation and interleukin (IL)-12 release. Infected DCs efficiently stimulate CD4- and CD8- T cells and vaccinate against leishmaniasis. In contrast, complement receptor 3-dependent phagocytosis of L. major by macrophages (MPhi) leads exclusively to MHC class II-restricted antigen presentation to primed, but not naive, T cells, and no IL-12 production. Herein, we demonstrate that uptake of L. major by DCs required parasite-reactive immunoglobulin (Ig)G and involved FcgammaRI and FcgammaRIII. In vivo, DC infiltration of L. major-infected skin lesions coincided with the appearance of antibodies in sera. Skin of infected B cell-de…

T cellImmunologyAntigen presentationLeishmaniasis CutaneousMacrophage-1 AntigenPriming (immunology)Complement receptorArticleImmunoglobulin GMicePhagocytosismedicineAnimalsImmunology and AllergyLeishmania majorCells CulturedLeishmania majorMice KnockoutB-LymphocytesMice Inbred BALB CbiologyMacrophagesReceptors IgGArticlesDendritic Cellsbiology.organism_classificationMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GImmunologybiology.proteinInterleukin 12CD8Journal of Experimental Medicine
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Beta-Catenin mediates tumor-induced immunosuppression by inhibiting cross-priming of CD8(+) T cells

2014

Tumors activate -catenin in DCs to suppress CD8 immunity by inhibiting cross-priming; -catenin-suppressed CD8 immunity could be rescued by enhancing cross-priming. Whereas CD8(+) T cells are essential for anti-tumor immunity, tumors often evade CD8(+) T cell surveillance by immunosuppression. As the initiators of antigen-specific immune responses, DCs are likely to play a central role in regulating the balance between immunity and tolerance to tumor antigens and are specialized in their ability to cross-present exogenous tumor antigens on MHC class I molecules to initiate CD8(+) T cell immunity. However, it remains unclear whether and how tumors modulate DC functions to suppress CD8(+) T ce…

T cellImmunologyMelanoma ExperimentalPriming (immunology)chemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesImmune toleranceMiceImmune systemCross-PrimingAntigenSDG 3 - Good Health and Well-beingImmunityNeoplasmsMHC class ImedicineImmune ToleranceImmunology and AllergyCytotoxic T cellAnimalsbeta CateninMice KnockoutCell BiologyDendritic Cellsmedicine.anatomical_structureImmunologyCancer researchbiology.proteinImmunologic Memory
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The mitochondrial protein TCAIM regulates activation of T cells and thereby promotes tolerance induction of allogeneic transplants.

2013

Primary T cell activation and effector cell differentiation is required for rejection of allogeneic grafts in naive recipients. It has become evident, that mitochondria play an important role for T cell activation. Expression of several mitochondrial proteins such as TCAIM (T cell activation inhibitor, mitochondrial) is down-regulated upon T cell receptor triggering. Here we report that TCAIM inhibited spontaneous development of memory and effector T cells. CD4(+) T cells from Tcaim knock-in (KI) mice showed reduced activation, cytokine secretion and proliferation in vitro. Tcaim KI T cells tolerated allogeneic skin grafts upon transfer into Rag-1 KO mice. CD4(+) and CD8(+) T cells from the…

T cellT-LymphocytesBiologyLymphocyte ActivationT-Lymphocytes RegulatoryMitochondrial ProteinsInterleukin 21MicemedicineImmunology and AllergyCytotoxic T cellAnimalsTransplantation HomologousPharmacology (medical)IL-2 receptorAntigen-presenting cellCells CulturedHomeodomain ProteinsMice KnockoutTransplantationMice Inbred BALB CZAP70CD28Cell DifferentiationSkin TransplantationFlow CytometryCell biologyMitochondriaMice Inbred C57BLmedicine.anatomical_structureCytokinesTransplantation ToleranceReactive Oxygen SpeciesImmunologic MemoryCD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
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Intrahepatic myeloid-cell aggregates enable local proliferation of CD8+T cells and successful immunotherapy against chronic viral liver infection

2013

Chronic infection is difficult to overcome because of exhaustion or depletion of cytotoxic effector CD8(+) T cells (cytotoxic T lymphoytes (CTLs)). Here we report that signaling via Toll-like receptors (TLRs) induced intrahepatic aggregates of myeloid cells that enabled the population expansion of CTLs (iMATEs: 'intrahepatic myeloid-cell aggregates for T cell population expansion') without causing immunopathology. In the liver, CTL proliferation was restricted to iMATEs that were composed of inflammatory monocyte-derived CD11b(+) cells. Signaling via tumor-necrosis factor (TNF) caused iMATE formation that facilitated costimulation dependent on the receptor OX40 for expansion of the CTL popu…

T cellmedicine.medical_treatmentImmunologyPopulationGreen Fluorescent ProteinsMice TransgenicBiologyCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisMicemedicineImmunology and AllergyCytotoxic T cellAnimalsLymphocytic choriomeningitis virusMyeloid CellseducationCell ProliferationMice Knockouteducation.field_of_studyLiver infectionCD11b AntigenMicroscopy ConfocalLiver DiseasesImmunotherapyReceptors OX40Flow CytometryMice Inbred C57BLCTL*Chronic infectionmedicine.anatomical_structureAnimals NewbornLiverToll-Like Receptor 9ImmunologyChronic DiseaseHost-Pathogen InteractionsImmunotherapyCD8Signal TransductionT-Lymphocytes CytotoxicNature Immunology
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Cutting Edge: IL-23 Cross-Regulates IL-12 Production in T Cell-Dependent Experimental Colitis

2006

Abstract Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. …

T-LymphocytesTransgeneT cellImmunologyDown-RegulationMice TransgenicInterleukin-23PathogenesisMiceInterleukin 23AnimalsImmunology and AllergyMedicineColitisCells Culturedbusiness.industryInterleukinsExperimental autoimmune encephalomyelitisColitismedicine.diseaseInterleukin-12Survival RateDisease Models AnimalProtein Subunitsmedicine.anatomical_structureImmunologyKnockout mouseInterleukin-23 Subunit p19Interleukin 12Disease SusceptibilitybusinessThe Journal of Immunology
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Cutting Edge: A Key Pathogenic Role of IL-27 in T Cell- Mediated Hepatitis

2007

Abstract The signals driving T cell activation in T cell-mediated fulminant hepatitis are not fully understood. In this study, we identify the cytokine IL-27p28/EBI3 as a major pathogenic factor in the ConA model of T cell-mediated hepatitis. We found an up-regulation of hepatic EBI3 and p28 expression and augmented levels of IL-27 in wild-type mice after ConA administration, suggesting a potential pathogenic role of this cytokine in ConA hepatitis. Consistently, IL-27 EBI3-deficient mice were almost completely protected from ConA-induced liver damage. Such protection was associated with reduced levels of IFN-γ and its signaling proteins pSTAT-1 and T-bet. Finally, in vivo blockade of IL-27…

T-Lymphocytesmedicine.medical_treatmentT cellImmunologychemical and pharmacologic phenomenaBiologyMinor Histocompatibility AntigensInterferon-gammaMiceConcanavalin AmedicineAnimalsImmunology and AllergyReceptors CytokineReceptorFulminant hepatitisMice KnockoutHepatitisLiver injuryInterleukin-17EBI3medicine.diseaseUp-RegulationSTAT1 Transcription FactorCytokinemedicine.anatomical_structureImmunologyChemical and Drug Induced Liver InjurySignal transductionSignal TransductionThe Journal of Immunology
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