Search results for "Knockout"

showing 10 items of 806 documents

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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Binding to complement factors and activation of the alternative pathway by Acanthamoeba.

2010

Acanthamoeba can cause severe ocular and cerebral diseases in healthy and immunocompromised individuals, respectively. Activation of complement appears to play an important role in host defence against infection. The exact mechanism, however, is still unclear. The aim of the present study was to investigate the effect of normal human serum (NHS) and normal mouse serum (NMS) on Acanthamoeba trophozoites, the binding of different complement factors to Acanthamoeba and the activation of the complement system. Moreover, we aimed to work out any possible differences between different strains of Acanthamoeba. A virulent T4 strain, a non-virulent T4 strain and a virulent T6 strain were included in…

ImmunologyComplement Pathway AlternativeVirulenceAcanthamoebaComplement factor IAntigen-Antibody ComplexImmunofluorescenceMannose-Binding LectinBacterial AdhesionMicrobiologyMiceSpecies Specificityparasitic diseasesmedicineImmunology and AllergyAnimalsHumansTrophozoitesIncubationEdetic AcidMice Knockoutmedicine.diagnostic_testbiologyVirulenceComplement C1qHematologyAmebiasisComplement C3biology.organism_classificationComplement C9Complement systemAcanthamoebaMice Inbred C57BLAlternative complement pathwayIntracellularImmunobiology
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Specific and Redundant Roles for NFAT Transcription Factors in the Expression of Mast Cell-Derived Cytokines

2006

Abstract By virtue of their ability to express a plethora of biologically highly active mediators, mast cells (MC) are involved in both adaptive and innate immune responses. MC-derived Th2-type cytokines are thought to act as local amplifiers of Th2 reactions, including chronic inflammatory disorders such as allergic asthma, whereas MC-derived TNF-α is a critical initiator of antimicrobial defense. In this study, we demonstrate that the transcription factors NFATc1 and NFATc2 are part of a MC-specific signaling network that regulates the expression of TNF-α and IL-13, whereas NFATc3 is dispensable. Primary murine bone marrow-derived MC from NFATc2−/− mice, activated by either ionomycin or I…

ImmunologyDown-RegulationImmunoglobulin EMicechemistry.chemical_compoundTh2 CellsCell Line TumormedicineAnimalsImmunology and AllergyMast CellsTranscription factorCells CulturedMice KnockoutMice Inbred BALB CGene knockdownInterleukin-13Innate immune systemNFATC Transcription FactorsbiologyTumor Necrosis Factor-alphaDegranulationNFATMast cellUp-RegulationCell biologymedicine.anatomical_structurechemistryIonomycinImmunologybiology.proteinCytokinesThe Journal of Immunology
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Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection.

2015

The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-λ (IFN-λ), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-λ, both of which were 'preferentially' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These d…

ImmunologyImmunoblottingMolecular Sequence DataGene ExpressionMice Transgenicmedicine.disease_causeRotavirus InfectionsCell LineMadin Darby Canine Kidney CellsInterleukin 22DogsInterferonRotavirusChlorocebus aethiopsmedicineImmunology and AllergyAnimalsHumansSTAT1Intestinal MucosaReceptors CytokineVero CellsMice KnockoutbiologyReverse Transcriptase Polymerase Chain ReactionInterleukinsInnate lymphoid cellInterleukinDrug SynergismEpithelial CellsVirology3. Good healthIntestinesMice Inbred C57BLSTAT1 Transcription FactorViral replicationImmunologybiology.proteinVero cellCytokinesCaco-2 CellsHT29 Cellsmedicine.drugNature immunology
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Secreted proteophosphoglycan of Leishmania mexicana amastigotes activates complement by triggering the mannan binding lectin pathway.

1997

Cutaneous lesions induced by infection of mice with the protozoan parasite, Leishmania mexicana, contain abundant amounts of a high molecular mass proteophosphoglycan (PPG), which is secreted by the amastigote stage residing in phagolysosomes of macrophages and can then be released into the tissue upon rupture of the infected cells. Amastigote PPG forms sausage-shaped but soluble particles and belongs to a novel class of serine-rich proteins that are extensively O-glycosylated by phosphooligosaccharides capped by mannooligosaccharides. The purified molecule is shown here to efficiently activate complement (C) and deplete hemolytic activity of normal serum and may prevent the opsonization of…

ImmunologyLeishmania mexicanaProtozoan ProteinsCollectinLeishmaniasis CutaneousLeishmania mexicanaMiceImmunology and AllergyAnimalsAmastigoteComplement ActivationMannan-binding lectinSerine proteaseMice KnockoutbiologyMacrophagesComplement C4Complement C3biology.organism_classificationCollectinsComplement systemAntibody opsonizationBiochemistryLectin pathwaybiology.proteinMice Inbred CBACalciumProteoglycansCarrier ProteinsEuropean journal of immunology
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Human Siglec-10 can bind to vascular adhesion protein-1 and serves as its substrate

2009

AbstractLeukocytes migrate from the blood into areas of inflammation by interacting with various adhesion molecules on endothelial cells. Vascular adhesion protein-1 (VAP-1) is a glycoprotein expressed on inflamed endothelium where it plays a dual role: it is both an enzyme that oxidizes primary amines and an adhesin that is involved in leukocyte trafficking to sites of inflammation. Although VAP-1 was identified more than 15 years ago, the counterreceptor(s) for VAP-1 on leukocytes has remained unknown. Here we have identified Siglec-10 as a leukocyte ligand for VAP-1 using phage display screenings. The binding between Siglec-10 and VAP-1 was verified by different adhesion assays, and this…

ImmunologyReceptors Cell SurfaceInflammationCHO CellsPlasma protein bindingBiologyLigandsBiochemistryMice03 medical and health sciencesCricetulus0302 clinical medicinePeptide LibraryVascular BiologyCricetinaeLectinsLeukocyte TraffickingCell AdhesionmedicineAnimalsHumansEndotheliumLymphocytesProtein Structure QuaternaryCell adhesion030304 developmental biologyMice Knockout0303 health sciencesCell adhesion moleculeSoluble cell adhesion moleculesSIGLECCell BiologyHematologyAdhesionrespiratory systembacterial infections and mycosesRecombinant Proteinsrespiratory tract diseasesChemotaxis LeukocyteBiochemistry030220 oncology & carcinogenesisAmine Oxidase (Copper-Containing)medicine.symptomCell Adhesion MoleculesProtein BindingBlood
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Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida al…

2008

Candida albicans is the major cause of systemic fungal infections in immunocompromised patients. We investigated the susceptibility of mice deficient in complement factor B and C2 (Bf/C2-/-), C1q (C1qa-/-), and mannan-binding lectin (MBL)-A (MBL-A) and MBL-C (MBL-A/C-/-) to systemic infection with C. albicans. Animals were infected i.p. with 10(8)C. albicans blastoconidia and monitored for mortality. Bf/C2-/- mice showed high mortality (over 90%) within the study period of 3 weeks. In contrast, mortality in C1qa-/- mice was below 15% whereas that of MBL-A/C-/- mice was 40% (P0.001). Intravenous infection of mice with 8x10(5) blastoconidia resulted in the same trend with Bf/C2-/- mice being …

Immunologychemical and pharmacologic phenomenaOpportunistic InfectionsMannose-Binding LectinBlastoconidiumComplement factor BMicrobiologyMicePhagocytosisSpecies SpecificityCandida albicansAnimalsGenetic Predisposition to DiseaseCandida albicansDouble knockoutComplement ActivationMolecular BiologyMannan-binding lectinMice KnockoutbiologyCandidiasisLectinComplement Pathway Mannose-Binding LectinComplement C2bacterial infections and mycosesbiology.organism_classificationCorpus albicansKnockout mousebiology.proteinComplement Factor BMolecular Immunology
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Fertility Relevance Probability Analysis Shortlists Genetic Markers for Male Fertility Impairment.

2020

Impairment of male fertility is one of the major public health issues worldwide. Nevertheless, genetic causes of male sub- and infertility can often only be suspected due to the lack of reliable and easy-to-use routine tests. Yet, the development of a marker panel is complicated by the large quantity of potentially predictive markers. Actually, hundreds or even thousands of genes could have fertility relevance. Thus, a systematic method enabling a selection of the most predictive markers out of the many candidates is required. As a criterion for marker selection, we derived a gene-specific score, which we refer to as fertility relevance probability (FRP). For this purpose, we first categori…

InfertilityGenetic MarkersMalemedia_common.quotation_subjectFertilityBiologyLogistic regressionMale infertility03 medical and health sciencesDAZLMiceTestisGeneticsmedicineAnimalsHumansAmino Acid SequenceMolecular BiologyGeneGenetics (clinical)Genetic Association StudiesInfertility Male030304 developmental biologymedia_commonProbabilityGeneticsMice Knockout0303 health sciences030305 genetics & hereditymedicine.diseasePhenotypeLogistic ModelsGenetic markerCytogenetic and genome research
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CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

2021

BACKGROUND: CD248 is a pro-inflammatory, transmembrane glycoprotein expressed by vascular smooth muscle cells (VSMC), monocytes/macrophages, and other cells of mesenchymal origin. Its distribution and properties are reminiscent of those of the initiator of coagulation, tissue factor (TF). OBJECTIVE: We examined whether CD248 also participates in thrombosis. METHODS: We evaluated the role of CD248 in coagulation using mouse models of vascular injury, and by assessing its functional interaction with the TF-factor VIIa (FVIIa)-factor X (FX) complex. RESULTS: The time to ferric chloride-induced occlusion of the carotid artery in CD248 knockout (KO) mice was significantly longer than in wild-typ…

InflammationFactor VIIa030204 cardiovascular system & hematologyInferior vena cavaArticleThromboplastin03 medical and health sciencesTissue factorchemistry.chemical_compoundMice0302 clinical medicineThrombinTissue factor pathway inhibitorAntigens CDAntigens NeoplasmmedicineAnimalsHumansMice KnockoutVenous Thrombosismedicine.diagnostic_testFactor XHematologyCoagulationchemistrymedicine.veinCancer researchProthrombin Timemedicine.symptommedicine.drugPartial thromboplastin time
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Role of NF-kappaB in immune and inflammatory responses in the gut.

1998

NF-kappaB is a pleiotropic transcription factor with key functions in the intestinal immune system. NF-kappaB family members control transcriptional activity of various promoters of proinflammatory cytokines, cell surface receptors, transcription factors, and adhesion molecules that are involved in intestinal inflammation. The perpetuated activation of NF-kappaB in patients with active inflammatory bowel disease suggests that regulation of NF-kappaB activity is a very attractive target for therapeutic intervention. Such strategies include antioxidants, proteasome inhibitors, inhibition of NF-kappaB by adenoviral I kappaB alpha expression vectors, and antisense DNA targeting of NF-kappaB. Th…

InflammationMice KnockoutGastroenterologyNF-kappa BInflammationPromoterReviewBiologyNFKB1Proinflammatory cytokineIκBαIntestinal DiseasesMiceImmune systemProteasomeImmunologymedicineAnimalsHumansmedicine.symptomTranscription factorSignal TransductionTranscription FactorsGut
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