Search results for "Innate"

showing 10 items of 638 documents

Changes in immunohistochemical levels and subcellular localization after therapy and correlation and colocalization with CD68 suggest a pathogenetic …

2011

In an earlier work, the role of heat shock protein (Hsp60) in the pathogenesis of ulcerative colitis (UC) was suggested by its significant increase in the pathological mucosa parallel with an increase in inflammatory cells. More data in this direction are reported in this work. We analyzed by immunohistochemistry biopsies of colon tissue from 2 groups of patients with UC and treated with either 5-aminosalicylic acid (5-ASA) alone or in combination with a probiotic. We looked for inflammatory markers and Hsp60. Both the treatments were effective in reducing symptoms but the group treated with both 5-ASA and probiotics showed better clinical results. Amelioration of symptoms was associated wi…

Hsp60 chaperonin ulcerative colitis macrophages CD68 inflammation innate immunity
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The viral chemokine MCK-2 of murine cytomegalovirus promotes infection as part of a gH/gL/MCK-2 complex.

2013

Human cytomegalovirus (HCMV) forms two gH/gL glycoprotein complexes, gH/gL/gO and gH/gL/pUL(128,130,131A), which determine the tropism, the entry pathways and the mode of spread of the virus. For murine cytomegalovirus (MCMV), which serves as a model for HCMV, a gH/gL/gO complex functionally homologous to the HCMV gH/gL/gO complex has been described. Knock-out of MCMV gO does impair, but not abolish, virus spread indicating that also MCMV might form an alternative gH/gL complex. Here, we show that the MCMV CC chemokine MCK-2 forms a complex with the glycoprotein gH, a complex which is incorporated into the virion. We could additionally show that mutants lacking both, gO and MCK-2 are not ab…

Human cytomegalovirusViral DiseasesMuromegalovirusChemokinevirusesMurine Cytomegalovirus ; viral chemokine MCK-2 ; gH/gL/MCK-2 complexMiceViral Envelope ProteinsBiology (General)Cells Culturedchemistry.chemical_classificationMice Inbred BALB Cvirus diseasesHerpesviridae InfectionsRecombinant ProteinsSpecific Pathogen-Free OrganismsInfectious DiseasesLiverChemokines CCMedicineFemaleResearch ArticleQH301-705.5ImmunologyBiologyMicrobiologyVirusCell LineViral ProteinsMuromegalovirusGlycoprotein complexVirologyGeneticsmedicineAnimalsBiologyMolecular BiologyTropismMacrophagesVirionVirus InternalizationRC581-607medicine.diseasebiology.organism_classificationVirologyImmunity InnatechemistryCell cultureMutationMacrophages Peritonealbiology.proteinParasitologyProtein MultimerizationImmunologic diseases. AllergyGlycoprotein
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Differential disease resistance response in the barley necrotic mutant nec1

2010

Abstract Background Although ion fluxes are considered to be an integral part of signal transduction during responses to pathogens, only a few ion channels are known to participate in the plant response to infection. CNGC4 is a disease resistance-related cyclic nucleotide-gated ion channel. Arabidopsis thaliana CNGC4 mutants hlm1 and dnd2 display an impaired hypersensitive response (HR), retarded growth, a constitutively active salicylic acid (SA)-mediated pathogenesis-related response and elevated resistance against bacterial pathogens. Barley CNGC4 shares 67% aa identity with AtCNGC4. The barley mutant nec1 comprising of a frame-shift mutation of CNGC4 displays a necrotic phenotype and co…

Hypersensitive responseGeneticsbiologyMutantfood and beveragesCyclic Nucleotide-Gated Cation ChannelsPseudomonas syringaeBlumeria graminisHordeumPlant SciencePlant disease resistancebiology.organism_classificationImmunity Innatelcsh:QK1-989MicrobiologyFrameshift mutationAscomycotaInteraction with hostlcsh:BotanyPseudomonas syringaeFrameshift MutationPathogenPlant DiseasesPlant ProteinsResearch ArticleBMC Plant Biology
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Characterization of a new, nonpathogenic mutant of Botrytis cinerea with impaired plant colonization capacity.

2006

International audience; Botrytis cinerea is a necrotrophic pathogen that attacks more than 200 plant species.Here, the nonpathogenic mutant A336, obtained via insertional mutagenesis, was characterized.Mutant A336 was nonpathogenic on leaves and fruits, on intact and wounded tissue, while still able to penetrate the host plant. It grew normally in vitro on rich media but its conidiation pattern was altered. The mutant did not produce oxalic acid and exhibited a modified regulation of the production of some secreted proteins (acid protease 1 and endopolygalacturonase 1). Culture filtrates of the mutant triggered an important oxidative burst in grapevine ( Vitis vinifera ) suspension cells, a…

Hypersensitive responsehypersensitive responsePhysiology[SDV]Life Sciences [q-bio]colonisationMutantArabidopsisConidiationPlant ScienceMicrobiologyInsertional mutagenesisFungal Proteins03 medical and health sciencesPlasmidGene Expression Regulation FungalOnionsBotrytis cinerea; endopolygalacturonase BcPG1; hypersensitive responseVitismutantoxidative burstPathogenGene030304 developmental biologyBotrytis cinereaPhaseolus0303 health sciencesoxalateendopolygalacturonase BcPG1biology030306 microbiologyOxalic Acidfungifood and beveragesHydrogen-Ion Concentrationbiology.organism_classificationImmunity Innatenonpathogenic mutantEnzymesPlant LeavesMutagenesis Insertionalnonaspartyl acid protease ACP1Mutationbotrytis cinerea;endopolygalacturonase BcPG1;hypersensitive response;nonaspartyl acid protease ACP1;nonpathogenic mutant;oxalate;oxidative burstBotrytisbotrytis cinereaReactive Oxygen SpeciesThe New phytologist
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TLR2, but not TLR4, triggers cytokine production by murine cells in response to Candida albicans yeasts and hyphae.

2006

Toll-like receptors (TLRs) function as sensors for infection that induce the activation of the immune responses. Recent studies have demonstrated a crucial involvement of TLRs in the recognition of fungal pathogens such as Candida albicans. Although both TLR2 and TLR4 have been implicated in the host interaction with C. albicans, their specific role during infection has not been unequivocally established, as conflicting results have been reported. In this review, we summarize and discuss our own and others' key findings about the specific role of TLR2 and TLR4 in murine resistance to candidiasis, and in triggering cytokine secretion by murine cells in response to C. albicans yeasts and hyph…

Hyphamedicine.medical_treatmentImmunologyHyphaeBiologyMicrobiologyModels BiologicalMicrobiologyMiceImmune systemCandida albicansmedicineAnimalsCandida albicansToll-like receptorCandidiasisbiology.organism_classificationCorpus albicansImmunity InnateToll-Like Receptor 2Toll-Like Receptor 4TLR2Infectious DiseasesCytokineImmunologyCytokinesCytokine secretionMicrobes and infection
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Toll-like receptors – sentries in the B-cell response

2009

Summary Toll-like receptors (TLR) play a central role in the initiation of the innate immune response to pathogens. Upon recognition of molecular motifs specific for microbial molecules TLR mediate pro-inflammatory cytokine secretion and enhance antigen presentation; in B cells they further promote expansion, class switch recombination and immunoglobulin secretion. As a result of their adjuvant properties, TLR ligands have become an integral component of antimicrobial vaccines. In spite of this, little is known of the direct effects of TLR engagement on B-lymphocyte function. The scope of this review is to outline the differences in TLR expression and reactivity in murine and human B-cell s…

ImmunologyAntigen presentationReview ArticleBiologyImmunoglobulin secretionImmunomodulationMicemedicineImmunology and AllergyAnimalsHumansReceptorB cellB-LymphocytesInnate immune systemToll-Like ReceptorsImmunoglobulin Class SwitchingImmunity InnateCell biologymedicine.anatomical_structureImmunoglobulin class switchingImmunologyAntibody FormationHost-Pathogen InteractionsCytokine secretionFunction (biology)
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Cyclic adenosine monophosphate and IL-10 coordinately contribute to nTreg cell-mediated suppression of dendritic cell activation

2010

In humans and mice naturally occurring regulatory T cells (nTregs) are crucial for the maintenance of peripheral tolerance by controlling not only potentially autoreactive T cells but virtually all cells of the adaptive and innate immune system. Here we show that co-culture of murine dendritic cells (DC) and nTregs results in an immediate increase of cAMP in DC, responsible for a rapid down-regulation of co-stimulatory molecules (CD80, CD86). In addition, the inhibitory surface molecule B7-H3 on DC is up-regulated. Subsequently, nTreg-derived IL-10 inhibits the cytokine production (IL-6, IL-12) of suppressed DC therewith preserving their silent phenotype. Hence, our data indicate that nTreg…

ImmunologyDown-RegulationCell CommunicationBiologyT-Lymphocytes RegulatoryImmune toleranceMiceImmune systemCyclic AMPImmune ToleranceAnimalsCD86Innate immune systemInterleukin-6Peripheral toleranceDendritic CellsDendritic cellInterleukin-12Coculture TechniquesInterleukin-10Cell biologyInterleukin 10B7-1 AntigenB7-2 AntigenCD80Signal TransductionCellular Immunology
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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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Altered metabolism of gut microbiota contributes to chronic immune activation in HIV-infected individuals.

2015

Altered interplay between gut mucosa and microbiota during treated HIV infection may possibly contribute to increased bacterial translocation and chronic immune activation, both of which are predictors of morbidity and mortality. Although a dysbiotic gut microbiota has recently been reported in HIV + individuals, the metagenome gene pool associated with HIV infection remains unknown. The aim of this study is to characterize the functional gene content of gut microbiota in HIV + patients and to define the metabolic pathways of this bacterial community, which is potentially associated with immune dysfunction. We determined systemic markers of innate and adaptive immunity in a cohort of HIV-in…

ImmunologyHIV InfectionsBiologyGut floraAdaptive ImmunityMicrobiologyMetabolomicsImmunityAntiretroviral Therapy Highly ActiveRNA Ribosomal 16SMetabolomeImmunology and AllergyCluster AnalysisHumansMetabolomicsGeneCase-control studyBayes TheoremBiodiversityAcquired immune systembiology.organism_classificationImmunity InnateMarkov ChainsGastrointestinal MicrobiomeMetabolic pathwayCase-Control StudiesImmunologyDisease ProgressionHIV-1MetabolomeMetagenomeMucosal 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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