Search results for "Knockout"

showing 10 items of 806 documents

Asthmatic changes in mice lacking T-bet are mediated by IL-13

2005

Mice with a targeted deletion of the T-bet gene exhibit spontaneous airway hyperresponsiveness (AHR), airway inflammation, enhanced recovery of T(h)2 cytokines from bronchoalveolar lavage fluid, sub-epithelial collagen deposition and myofibroblast transformation. Here we analyze the mechanisms responsible for the chronic airway remodeling observed in these mice. CD4+ T cells isolated from the lung of T-bet-deficient mice were spontaneously activated CD44(high)CD69(high) memory T cells, with a typical T(h)2 cytokine profile. Neutralization of IL-13 but not IL-4 resulted in amelioration of AHR in airways of mice lacking T-bet. IL-13 blockade also led to reduced eosinophilia and decreased vime…

CD4-Positive T-LymphocytesImmunologychemical and pharmacologic phenomenaVimentinLymphocyte ActivationSmad7 ProteinMiceTransforming Growth Factor betamedicineAnimalsVimentinImmunology and AllergyEosinophiliaSmad3 ProteinLungCells CulturedMice KnockoutInterleukin-13Lungbiologymedicine.diagnostic_testChemistryCD69hemic and immune systemsGeneral MedicineTransforming growth factor betaFibroblastsrespiratory systemActinsAsthmarespiratory tract diseasesDNA-Binding ProteinsMice Inbred C57BLBronchoalveolar lavagemedicine.anatomical_structureInterleukin 13ImmunologyTrans-Activatorsbiology.proteinCytokinesInterleukin-4medicine.symptomT-Box Domain ProteinsImmunologic MemoryMyofibroblastTranscription FactorsInternational Immunology
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The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.

2015

The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and …

CD4-Positive T-LymphocytesInflammasomesImmunologyBlotting WesternBiologyInterleukin 21MiceTh2 CellsCell Line TumorNLR Family Pyrin Domain-Containing 3 ProteinImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPromoter Regions GeneticInterleukin 3Oligonucleotide Array Sequence AnalysisMice KnockoutCD40integumentary systemReverse Transcriptase Polymerase Chain ReactionZAP70Gene Expression ProfilingCell DifferentiationNeoplasms ExperimentalAsthmaCell biologyGene Expression Regulation NeoplasticMice Inbred C57BLInterleukin 10Interferon Regulatory FactorsInterleukin 12biology.proteinNIH 3T3 CellsTrans-ActivatorsFemaleInterleukin-4Carrier ProteinsProtein BindingSignal TransductionNature immunology
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Adoptive transfer of protective immunity from Cryptosporidium parvum-infected interferon-gamma and interleukin-12-deficient mice to naive recipients.

2008

We investigated the possibility of transfer immunity from Cryptosporidium parvum-infected interferon-gamma (GKO) and interleukin-12p40 (IL-12KO) deficient C57BL/6 mice to naive mice by transfer of intraepithelial lymphocytes (IELs) and CD4(+) T cells from spleen and mesenteric lymph nodes (MLNs). Three days after the transfer recipients were infected with C. parvum. IELs isolated from GKO donor mice after resolution of infection (day 15) but not at the peak of infection (day 8) significantly reduced the parasite load in recipient mice. In IL-12KO mice, IELs and also CD4(+) T cells isolated from the spleen and MLNs of donor mice at the peak of infection (day 5) and after resolution (day 15) …

CD4-Positive T-LymphocytesMaleAdoptive cell transferCryptosporidiosisSpleenHost-Parasite InteractionsInterferon-gammaMiceImmunityCell Movementparasitic diseasesmedicineMesenteric lymph nodesAnimalsImmunity MucosalCryptosporidium parvumMice KnockoutGeneral VeterinaryGeneral Immunology and MicrobiologybiologyImmunomagnetic SeparationPublic Health Environmental and Occupational Healthbiology.organism_classificationAdoptive TransferInterleukin-12Mice Inbred C57BLInfectious Diseasesmedicine.anatomical_structureCryptosporidium parvumAdoptive immunityImmunologyInterleukin 12Molecular MedicineIntraepithelial lymphocyteFemaleLymph NodesSpleenVaccine
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The Programmed Death (PD)‐1/PD‐Ligand 1 Pathway Regulates Graft‐Versus‐Host‐Reactive CD8 T Cells After Liver Transplantation

2008

Acute graft-versus-host disease (aGVHD) is a life-threatening complication after solid-organ transplantation, which is mediated by host-reactive donor T cells emigrating from the allograft. We report on two liver transplant recipients who developed an almost complete donor chimerism in peripheral blood and bone marrow-infiltrating T cells during aGVHD. By analyzing these T cells directly ex vivo, we found that they died by apoptosis over time without evidence of rejection by host T cells. The host-versus-donor reactivity was selectively impaired, as anti-third-party and antiviral T cells were still detectable in the host repertoire. These findings support the acquired donor-specific allotol…

CD4-Positive T-LymphocytesMaleCell TransplantationProgrammed Cell Death 1 ReceptorGraft vs Host DiseaseCD8-Positive T-LymphocytesTCIRG1MiceInterleukin 21Immune systemAntigenAntigens CDAnimalsHumansImmunology and AllergyCytotoxic T cellMedicinePharmacology (medical)IL-2 receptorMice KnockoutTransplantationbusiness.industryInterleukin-2 Receptor alpha SubunitForkhead Transcription FactorsMiddle AgedLiver TransplantationTransplantationsurgical procedures operativeGene Expression RegulationAntigens SurfaceImmunologyInterleukin 12Apoptosis Regulatory ProteinsbusinessImmunosuppressive AgentsAmerican Journal of Transplantation
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Deficiency in the Transcription Factor Interferon Regulatory Factor (Irf)-2 Leads to Severely Compromised Development of Natural Killer and T Helper …

2000

Interferon (IFN) regulatory factor (IRF)-2 was originally described as an antagonist of IRF-1–mediated transcriptional regulation of IFN-inducible genes. IRF-1−/− mice exhibit defective T helper type 1 (Th1) cell differentiation. We have used experimental leishmaniasis to show that, like IRF-1−/− mice, IRF-2−/− mice are susceptible to Leishmania major infection due to a defect in Th1 differentiation. Natural killer (NK) cell development is compromised in both IRF-1−/− and IRF-2−/− mice, but the underlying mechanism differs. NK (but not NK+ T) cell numbers are decreased in IRF-2−/− mice, and the NK cells that are present are immature in phenotype. Therefore, like IRF-1, IRF-2 is required for…

CD4-Positive T-LymphocytesMaleInterferon Regulatory Factor 2Cellular differentiationImmunologyLeishmaniasis CutaneousBiologyNitric OxideTh1MiceInterleukin 21Immune systemBone MarrowInterferonmedicineAnimalsImmunology and AllergyLymphocyte CountLeishmania majorInterleukin-15Mice KnockoutLeishmaniaMice Inbred BALB Cnatural killer cellsCell DifferentiationTh1 CellsInterleukin-12Cell biologyDNA-Binding ProteinsKiller Cells NaturalMice Inbred C57BLRepressor ProteinsDisease Models AnimalInterleukin 15interferon regulatory factorImmunologyInterleukin 12FemaleOriginal ArticleDisease SusceptibilityInterferon Regulatory Factor-2interleukin 15Transcription FactorsInterferon regulatory factorsmedicine.drugJournal of Experimental Medicine
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IFN-γ–Producing CD4+ T Cells Promote Generation of Protective Germinal Center–Derived IgM+ B Cell Memory against Salmonella Typhi

2014

Abstract Abs play a significant role in protection against the intracellular bacterium Salmonella Typhi. In this article, we investigated how long-term protective IgM responses can be elicited by a S. Typhi outer-membrane protein C– and F–based subunit vaccine (porins). We found that repeated Ag exposure promoted a CD4+ T cell–dependent germinal center reaction that generated mutated IgM-producing B cells and was accompanied by a strong expansion of IFN-γ–secreting T follicular helper cells. Genetic ablation of individual cytokine receptors revealed that both IFN-γ and IL-17 are required for optimal germinal center reactions and production of porin-specific memory IgM+ B cells. However, mor…

CD4-Positive T-LymphocytesMaleSalmonella VaccinesProtein subunitmedicine.medical_treatmentImmunologyCellBiologySalmonella typhiMicrobiologyInterferon-gammaMice03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansImmunology and AllergyTyphoid FeverReceptorB cell030304 developmental biologyMice KnockoutB-Lymphocytes0303 health sciencesGerminal centerSalmonella typhiGerminal Center3. Good healthVaccinationmedicine.anatomical_structureCytokineImmunoglobulin MbacteriaFemaleImmunologic Memory030215 immunologyThe Journal of Immunology
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Development of Abdominal Aortic Aneurysm Is Decreased in Mice with Plasma Phospholipid Transfer Protein Deficiency

2013

International audience; Plasma phospholipid transfer protein (PLTP) increases the circulating levels of proatherogenic lipoproteins, accelerates blood coagulation, and modulates inflammation. The role of PLTP in the development of abdominal aortic aneurysm (AAA) was investigated by using either a combination of mechanical and elastase injury at one site of mouse aorta (elastase model) or continuous infusion of angiotensin II in hyperlipidemic ApoE-knockout mice (Ang II model). With the elastase model, complete PLTP deficiency was associated with a significantly lower incidence and a lesser degree of AAA expansion. With the Ang II model, findings were consistent with those in the elastase mo…

CD4-Positive T-LymphocytesMalemedicine.medical_specialty[SDV]Life Sciences [q-bio]Inflammation030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineMice03 medical and health sciencesAortic aneurysmApolipoproteins E0302 clinical medicinemedicine.arteryPhospholipid transfer proteinInternal medicinemedicineAnimalsPhospholipid Transfer ProteinsPancreatic elastaseAorta030304 developmental biologyInflammationMice Knockout0303 health sciencesAortaPancreatic ElastaseAngiotensin IIMacrophagesElastasemedicine.diseaseAngiotensin IIElastinMice Inbred C57BL[SDV] Life Sciences [q-bio]EndocrinologyLiverImmunologybiology.proteincardiovascular systemCytokinesmedicine.symptomElastinAortic Aneurysm Abdominal
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Methotrexate specifically modulates cytokine production by T cells and macrophages in murine collagen-induced arthritis (CIA): a mechanism for methot…

1999

SUMMARYImmunosuppressive therapy with methotrexate (MTX) has been established as effective treatment for patients with rheumatoid arthritis. To analyse the therapeutic potential and mechanisms of action of MTX, we determined serum cytokine levels and cytokine production by splenic T cells and macrophages in untreated and MTX-treated mice. Furthermore, we assessed the role of MTX in a murine model of experimental arthritis induced by collagen type II (CIA). MTX reduced spontaneous and IL-15-induced tumour necrosis factor (TNF) production by splenic T cells but not by macrophages from healthy mice in vitro in a dose-dependent manner. In contrast, interferon-gamma (IFN-γ) production was less s…

CD4-Positive T-LymphocytesMalemusculoskeletal diseasesT-Lymphocytesmedicine.medical_treatmentImmunologyArthritisMice TransgenicSpleenInterferon-gammaMiceImmune systemAnimalsImmunology and AllergyMedicineheterocyclic compoundsInterferon gammaskin and connective tissue diseasesInterleukin 4Interleukin-15Mice KnockoutMice Inbred BALB CInterleukin-6Tumor Necrosis Factor-alphabusiness.industryMacrophagesOriginal ArticlesImmunotherapymedicine.diseaseArthritis ExperimentalMethotrexatemedicine.anatomical_structureCytokineMice Inbred DBAImmunologyCytokinesTumor necrosis factor alphaCollagenInterleukin-4businessImmunosuppressive AgentsSpleenmedicine.drug
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New candidates for CD4 T cell pathogenicity in experimental neuroinflammation and multiple sclerosis

2015

Multiple sclerosis is a chronic autoimmune demyelinating disease of the central nervous system, which is thought to be triggered by environmental factors in genetically susceptible individuals leading to activation of autoreactive T lymphocytes. Large multi-centre genome-wide association studies have identified multiple genetic risk loci in multiple sclerosis. In this study, we investigated T cell transcriptomic changes in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. We correlated these findings with the multiple sclerosis risk genes postulated by the most recent Immunochip analysis and found that multiple sclerosis susceptibility genes were significant…

CD4-Positive T-LymphocytesMice KnockoutEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEffectorMultiple sclerosisT cellExperimental autoimmune encephalomyelitisGenome-wide association studyMERTKBiologymedicine.diseaseMice Inbred C57BLMicemedicine.anatomical_structureImmunologymedicineDemyelinating diseaseAnimalsHumansGene Regulatory NetworksNeurology (clinical)NeuroinflammationBrain
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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