Search results for "Knockout"

showing 6 items of 806 documents

Dynamics of gut mucosal and systemic Th1/Th2 cytokine responses in interferon-gamma and interleukin-12p40 knock out mice during primary and challenge…

2009

Cryptosporidium parvum is an intracellular parasite causing enteritis which can become life-threatening in the immunocompromised host. CD4+ T cells and interferon (IFN)-gamma play dominant roles in host immune response to infection. However, effector mechanisms that are responsible for recovery from infection are poorly understood. In the present study we analyzed mice deficient in IFN-gamma or interleukin (IL)-12 in parallel to C57BL/6 wild type mice as models for murine cryptosporidiosis. Our results identified IFN-gamma as the key cytokine in the innate as well as adaptive immunity during primary and also challenge C. parvum infection. Furthermore, both Th1 and Th2 cytokines appear to co…

medicine.medical_treatmentImmunologyCryptosporidiosisBiologyInterferon-gammaMiceImmune systemTh2 CellsImmunityIleummedicineImmunology and AllergyAnimalsInterferon gammaCryptosporidium parvumMice KnockoutInterleukin-12 Subunit p40Interleukin-18InterleukinHematologyTh1 CellsAcquired immune systembiology.organism_classificationMice Inbred C57BLCytokineCryptosporidium parvumGene Expression RegulationGastric MucosaOrgan SpecificityImmunologyInterleukin 12medicine.drugImmunobiology
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Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis.

2015

Dendritic cells (DCs) are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The beta-catenin pathway has been suggested to promote a regulatory DC phenotype. The aim of this study was to unravel the role of beta-catenin signalling to control DC function in the autoimmune collagen-induced arthritis model (CIA). Deletion of beta-catenin specifically in DCs was achieved by crossing conditional knockout mice with a CD11c-Cre transgenic mouse line. Bone marrow-derived DCs (BMDCs) were generated and used to study the maturation profile of …

medicine.medical_treatmentT cellAntigen-Presenting Cellslcsh:Medicinechemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryImmune toleranceMiceImmune TolerancemedicineAnimalsHumansCytotoxic T cellAntigen-presenting celllcsh:ScienceCollagen Type IIbeta CateninMice KnockoutMultidisciplinarylcsh:Rhemic and immune systemsDendritic CellsDendritic cellArthritis ExperimentalToll-Like Receptor 2Toll-Like Receptor 4TLR2Cytokinemedicine.anatomical_structureImmunologyTh17 Cellslcsh:QCD8Research ArticleSignal TransductionPLoS ONE
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Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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Late Activation of Stress-activated Protein Kinases/c-Jun N-terminal Kinases Triggered by Cisplatin-induced DNA Damage in Repair-defective Cells

2011

Although stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) are rapidly activated by genotoxins, the role of DNA damage in this response is not well defined. Here we show that the SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK (Thr-183/Tyr-185) correlates with the level of cisplatin-DNA adducts at late times (16–24 h) after drug treatment in both human and mouse cells. Transfection of platinated plasmid DNA also caused SAPK/JNK activation. A defect in transcription-coupled nucleotide excision repair resting on a mutation in Cockayne syndrome group B protein promoted the late SAPK/JNK activation following cisplatin exposure. Signaling to SAPK/JNK was accompanied by act…

rho GTP-Binding ProteinsDNA RepairMAP Kinase Kinase 4DNA repairDNA damageDNA damage response; DNA repair; cisplatin-DNA adducts; SAPK/JNKp38 mitogen-activated protein kinasesAntineoplastic AgentsCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesDNA and ChromosomesBiologyBiochemistryAtaxia Telangiectasia Mutated ProteinsDNA AdductsMiceRadiation IonizingAnimalsHumansDNA Breaks Double-StrandedMolecular BiologyReplication protein ACells CulturedMice KnockoutKinaseTumor Suppressor ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyMolecular biologyDNA-Binding ProteinsEnzyme Activationc-Jun N-terminal kinasesbiology.proteinCisplatinSignal TransductionNucleotide excision repairJournal of Biological Chemistry
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An arthritogenic alphavirus uses the α1β1 integrin collagen receptor

2005

Ross River (RR) virus is an alphavirus endemic to Australia and New Guinea and is the aetiological agent of epidemic polyarthritis or RR virus disease. Here we provide evidence that RR virus uses the collagen-binding alpha1beta1 integrin as a cellular receptor. Infection could be inhibited by collagen IV and antibodies specific for the beta1 and alpha1 integrin proteins, and fibroblasts from alpha1-integrin-/- mice were less efficiently infected than wild-type fibroblasts. Soluble alpha1beta1 integrin bound immobilized RR virus, and peptides representing the alpha1beta1 integrin binding-site on collagen IV inhibited virus binding to cells. We speculate that two highly conserved regions with…

α1β1 integrinCollagen Type IVIntegrin alpha1IntegrinAlphavirusBiologyVirus ReplicationAntibodiesVirusIntegrin alpha1beta1Collagen receptorMiceRoss River virusVirologyRoss River virusAnimalsHumansMice KnockoutCollagen IVVirus receptorFibroblastsbiology.organism_classificationMolecular biologySolubilityIntegrin alpha Mbiology.proteinReceptors VirusIntegrin beta 6Receptors Adrenergic beta-1ReceptorHeLa CellsVirology
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